The document discusses adrenergic systems and sympathetic transmission. It describes how catecholamines like adrenaline, noradrenaline, and dopamine are synthesized from amino acids in the liver and nervous system. It also summarizes their storage, release, uptake, metabolism, and effects on receptors. The actions and uses of various adrenergic drugs like adrenaline, dopamine, and amphetamine are outlined.
This document discusses adrenergic agonists and antagonists. It defines adrenergic agonists as drugs that produce actions similar to epinephrine or norepinephrine by interacting with adrenergic receptors or increasing norepinephrine availability. Adrenergic antagonists are then discussed and categorized based on whether they act on alpha receptors, beta receptors, or both. Examples are provided for each category along with their effects and clinical uses.
The document discusses the adrenergic system and sympathetic responses. It describes the synthesis, storage, release and uptake of catecholamines like adrenaline. Catecholamines are synthesized from phenylalanine and tyrosine in the liver and stored in vesicles in nerve endings. They are released by nerve impulses and recaptured via neuronal and vesicular uptake pumps. Catecholamines act on alpha and beta adrenergic receptors and are metabolized by monoamine oxidase and catechol-O-methyltransferase. Examples of adrenergic drugs and their uses are also provided.
This document provides an overview of adrenergic drugs. It begins by discussing the endogenous catecholamines - norepinephrine, epinephrine, and dopamine - and their effects. It then classifies adrenergic receptors and describes the response of effector organs. The document proceeds to classify and describe the mechanisms and effects of various adrenergic drugs, including direct-acting, indirect-acting, and mixed sympathomemetics. It discusses individual drugs like epinephrine, norepinephrine, dopamine, isoproterenol, and clonidine. The document provides a detailed but technical summary of adrenergic pharmacology.
This document discusses adrenergic agonists and antagonists. It describes the synthesis, storage, release, and degradation of catecholamines like norepinephrine. It outlines the different subtypes of alpha and beta adrenergic receptors, their locations, and the effects of agonist binding. Key adrenergic drugs like epinephrine, norepinephrine, dopamine, and dobutamine are explained in terms of their mechanisms of action, therapeutic uses, dosages, and adverse effects. Interactions between adrenergic drugs and other medications are also noted.
This document discusses adrenergic agonists, which are drugs that act on pathways mediated by the endogenous catecholamines norepinephrine and epinephrine. These drugs target various steps in catecholamine synthesis, storage, release, binding, and removal and are used to treat conditions like hypertension, depression, shock, asthma, and angina. Adrenergic agonists are classified as direct-acting if they act directly on receptors, or indirect-acting if they increase catecholamine levels in the synapse. The document also describes the subtypes of alpha and beta adrenergic receptors, their locations, mechanisms of action, and the effects of prolonged receptor stimulation.
This document discusses catecholamines and their roles in the sympathetic nervous system. It details the pathways of catecholamine synthesis from tyrosine to epinephrine. It describes catecholamine receptors, uptake and metabolism. It lists target organs and effects of norepinephrine, epinephrine, and dopamine. Adrenergic drugs used to stimulate or block catecholamine receptors are also outlined.
Adrenergic drugs have many uses. They are used to increase the output of the heart, to raise blood pressure, and to increase urine flow as part of the treatment of shock. Adrenergics are also used as heart stimulants.
This document discusses the physiology and pharmacology of the sympathetic nervous system and its receptors. It begins by describing epinephrine as an important regulator of heart and vascular responses to exercise and stress. It then defines sympathomimetic drugs as those that mimic epinephrine's actions. The document goes on to detail the different alpha and beta receptor subtypes, their locations, and examples of agonists and antagonists. It discusses sympathetic neurotransmission and the mechanisms of drug-induced effects. Overall, the document provides a comprehensive overview of the sympathetic nervous system and its clinical applications.
This document discusses adrenergic agonists and antagonists. It defines adrenergic agonists as drugs that produce actions similar to epinephrine or norepinephrine by interacting with adrenergic receptors or increasing norepinephrine availability. Adrenergic antagonists are then discussed and categorized based on whether they act on alpha receptors, beta receptors, or both. Examples are provided for each category along with their effects and clinical uses.
The document discusses the adrenergic system and sympathetic responses. It describes the synthesis, storage, release and uptake of catecholamines like adrenaline. Catecholamines are synthesized from phenylalanine and tyrosine in the liver and stored in vesicles in nerve endings. They are released by nerve impulses and recaptured via neuronal and vesicular uptake pumps. Catecholamines act on alpha and beta adrenergic receptors and are metabolized by monoamine oxidase and catechol-O-methyltransferase. Examples of adrenergic drugs and their uses are also provided.
This document provides an overview of adrenergic drugs. It begins by discussing the endogenous catecholamines - norepinephrine, epinephrine, and dopamine - and their effects. It then classifies adrenergic receptors and describes the response of effector organs. The document proceeds to classify and describe the mechanisms and effects of various adrenergic drugs, including direct-acting, indirect-acting, and mixed sympathomemetics. It discusses individual drugs like epinephrine, norepinephrine, dopamine, isoproterenol, and clonidine. The document provides a detailed but technical summary of adrenergic pharmacology.
This document discusses adrenergic agonists and antagonists. It describes the synthesis, storage, release, and degradation of catecholamines like norepinephrine. It outlines the different subtypes of alpha and beta adrenergic receptors, their locations, and the effects of agonist binding. Key adrenergic drugs like epinephrine, norepinephrine, dopamine, and dobutamine are explained in terms of their mechanisms of action, therapeutic uses, dosages, and adverse effects. Interactions between adrenergic drugs and other medications are also noted.
This document discusses adrenergic agonists, which are drugs that act on pathways mediated by the endogenous catecholamines norepinephrine and epinephrine. These drugs target various steps in catecholamine synthesis, storage, release, binding, and removal and are used to treat conditions like hypertension, depression, shock, asthma, and angina. Adrenergic agonists are classified as direct-acting if they act directly on receptors, or indirect-acting if they increase catecholamine levels in the synapse. The document also describes the subtypes of alpha and beta adrenergic receptors, their locations, mechanisms of action, and the effects of prolonged receptor stimulation.
This document discusses catecholamines and their roles in the sympathetic nervous system. It details the pathways of catecholamine synthesis from tyrosine to epinephrine. It describes catecholamine receptors, uptake and metabolism. It lists target organs and effects of norepinephrine, epinephrine, and dopamine. Adrenergic drugs used to stimulate or block catecholamine receptors are also outlined.
Adrenergic drugs have many uses. They are used to increase the output of the heart, to raise blood pressure, and to increase urine flow as part of the treatment of shock. Adrenergics are also used as heart stimulants.
This document discusses the physiology and pharmacology of the sympathetic nervous system and its receptors. It begins by describing epinephrine as an important regulator of heart and vascular responses to exercise and stress. It then defines sympathomimetic drugs as those that mimic epinephrine's actions. The document goes on to detail the different alpha and beta receptor subtypes, their locations, and examples of agonists and antagonists. It discusses sympathetic neurotransmission and the mechanisms of drug-induced effects. Overall, the document provides a comprehensive overview of the sympathetic nervous system and its clinical applications.
Adrenergic agonist agents can be categorized as catecholamines or non-catecholamines. Catecholamines like epinephrine and norepinephrine cannot be used orally due to their short half-life and inability to cross the blood-brain barrier, while non-catecholamines like ephedrine can be used orally and cross the BBB due to their longer half-life. These agents act on alpha and beta adrenergic receptors and are used clinically as pressor agents, cardiac stimulants, bronchodilators, and more. Common adverse effects include anxiety, headache, and arrhythmias.
This presentation contains drugs which blocks the adrenergic system e.g receptor blockers like alpha and beta receptor antagonists, adrenergic neuron blocking agents in details.various animated pictures are also included to make the presentation interesting as well as i have used various diagrams and tables to have better understanding of the topic. Thank you.
This document discusses adrenergic receptors and modulators. It describes the sympathetic nervous system and neurotransmitters like norepinephrine, epinephrine, and dopamine. Norepinephrine is stored in synaptic vesicles and released via calcium-dependent fusion. Release can be modulated by prejunctional autoreceptors and heteroreceptors. There are alpha and beta adrenergic receptors which are G-protein coupled and have various effects. Drugs can affect receptors as agonists or antagonists and are used to treat conditions like hypertension and heart failure.
Adrenergic antagonists alpha and beta blockersZulcaif Ahmad
The document discusses various types of adrenergic receptor antagonists including alpha blockers like prazosin and terazosin which are used to treat hypertension and benign prostatic hyperplasia, as well as non-selective antagonists like phentolamine and beta blockers like propranolol which are used to treat conditions like hypertension, angina, and arrhythmias. The mechanisms, classifications, clinical uses and side effects of these different adrenergic antagonists are explained in detail across multiple pages.
Antiadrenergic drugs, also known as alpha blockers or alpha antagonists, work by blocking the effects of adrenaline and other related drugs at receptor sites. They occupy both alpha-1 and alpha-2 adrenergic receptors without activating them. Clinically, they are used to modify the responses of endogenous catecholamines like adrenaline and noradrenaline in both physiological and pathophysiological conditions. Common uses include treating pheochromocytoma, hypertension, Raynaud's disease, and benign prostatic hyperplasia. Individual drugs vary in their selectivity and duration of action at different receptor subtypes. Side effects may include postural hypotension, nasal congestion, and inhibition of ejac
The document discusses drugs that affect the autonomic nervous system, including adrenergic agents that stimulate the sympathetic nervous system and adrenergic blocking agents that inhibit sympathetic stimulation. It describes the locations and functions of alpha-1, alpha-2, and beta-1/2 receptors, examples of adrenergic drugs, their mechanisms of action and therapeutic uses, side effects, and nursing considerations.
The document discusses adrenergic drugs and their mechanisms of action. It notes that some adrenergic drugs act directly on adrenergic receptors to activate them, while others block receptor action. It provides tables listing examples of direct-acting, indirect-acting, and mixed-action adrenergic agonists. The document then discusses specific adrenergic drugs in more detail, including epinephrine, norepinephrine, isoproterenol, dopamine, dobutamine, oxymetazoline, phenylephrine, methoxamine, and clonidine. It explains their structures, receptor selectivities, and physiological effects.
This document discusses adrenergic agonists and antagonists. It begins by classifying adrenergic agonists as direct acting, mixed acting, or indirect acting. It then discusses specific alpha-1, alpha-2, beta-1, and beta-2 adrenergic receptor agonists like phenylephrine, clonidine, dobutamine, and terbutaline. It details their mechanisms of action and clinical indications. The document concludes by discussing classes of adrenergic antagonists including alpha receptor antagonists, beta receptor antagonists, and specific drugs like propranolol, prazocin, and yohimbine.
The document discusses adrenoceptor agonists and antagonists. It begins by providing an overview of the sympathetic nervous system and drugs that act on it. It then describes direct-acting sympathomimetic drugs that mimic norepinephrine and epinephrine by acting on alpha and beta receptors. Various agonists are discussed in depth, including their mechanisms of action, effects, uses, and adverse reactions. The document also covers adrenoceptor antagonists that block alpha and beta receptors, describing examples like prazosin and propranolol along with their clinical applications.
This document discusses non-catecholamine sympathomimetic drugs. It describes their general properties, classification based on receptor selectivity, and examples like ephedrine, pseudoephedrine, amphetamine, and tyramine. It covers the pharmacokinetics, pharmacodynamics, therapeutic uses, adverse effects and toxicity of these important non-catecholamine sympathomimetic drugs.
This document summarizes adrenergic agonists and antagonists. It describes the synthesis and metabolism of catecholamines like dopamine, norepinephrine, and epinephrine. It also discusses the different adrenergic receptor types (alpha and beta), their locations and functions. Various adrenergic drugs are classified and their mechanisms, effects, uses, and adverse effects outlined, including epinephrine, norepinephrine, dopamine, dobutamine, dopexamine, fenoldopam, phenylephrine, clonidine and others.
1. Prazosin is a potent and selective α1 adrenergic receptor blocker used to treat hypertension. It has a first-dose phenomenon that can cause severe hypotension, so the initial dose should be small.
2. Beta blockers block the effects of sympathetic stimulation by competitively blocking beta receptors. They are used to treat hypertension, angina, migraines, hyperthyroidism and other conditions. Common side effects include bradycardia, heart block, bronchospasm and hypoglycemia.
3. Drug interactions can occur between beta blockers and calcium channel blockers, local anesthetics, or bile acid sequestering resins which can affect absorption of the beta blockers
This document summarizes adrenergic agents and adrenergic-blocking agents. It describes how adrenergic agents mimic the effects of the sympathetic nervous system by stimulating alpha-adrenergic and beta-adrenergic receptors located throughout the body. It also describes how adrenergic-blocking agents, also called sympatholytics, inhibit the effects of the sympathetic nervous system by blocking these same receptors. Examples of different types of adrenergic and adrenergic-blocking agents are provided along with their therapeutic uses and important monitoring parameters.
This document discusses sympathomimetic drugs and adrenergic agonists. It describes how sympathomimetics mimic the effects of sympathetic nerve stimulation by acting on adrenergic receptors. It classifies adrenergic agonists as catecholamines or non-catecholamines and discusses their differences. It also summarizes the endogenous catecholamines, their synthesis, storage, and release. Additionally, it provides details on adrenergic receptors and the therapeutic uses, pharmacological actions, and side effects of various adrenergic drugs including epinephrine, dopamine, isoproterenol, dobutamine, ephedrine, and mephenteramine.
This document discusses various alpha and beta receptor antagonists. It provides details on their mechanisms of action, pharmacokinetics, clinical uses and side effects. Regarding alpha antagonists, it describes how they bind to alpha receptors to block catecholamine and sympathomimetic action. It also explains the differences between selective and non-selective alpha1 and alpha2 antagonists. For beta antagonists, it outlines their competitive inhibition of beta receptors and categorizes drugs as non-selective or cardioselective. The document discusses cardiovascular, respiratory, metabolic and other effects of both classes of drugs.
These are the drugs which antagonize the receptor action of adrenaline and related drugs.
These drugs act by blocking a and/or ß-adrenergic receptors.
α-blockers
PRAZOSIN is a competitive antagonist effective in the management of hypertension. Similar drugs with longer half-lives (e.g. doxazosin, terazosin).
β-blockers
Heart - Decrease heart rate, force of contraction and cardiac output.
Blood Pressure - Decrease in blood pressure (blockage).
Respiratory System – bronchoconstriction.
Eye – Beta-blocking agents reduce intraocular pressure, especially in glaucoma. The mechanism usually reported is decreased aqueous humor production.
Metabolic - Increase LDL and decrease HDL.
Uterus - Relaxation of uterus.
Local anaesthetic - Propranolol has some local anaesthetic action
This document discusses sympathomimetic drugs, which mimic the actions of epinephrine and norepinephrine. It describes the sympathetic and parasympathetic nervous systems, defines sympathomimetic drugs, and classifies them based on their mechanisms of action. The document also discusses the synthesis, storage, release, reuptake, and metabolism of catecholamines. It describes adrenergic receptors, where they are located, and provides examples of drugs that act on different receptor types. The actions and uses of epinephrine, norepinephrine, and dopamine are explained. Therapeutic classifications and examples of sympathomimetic drugs are also provided.
Adrenergic agonists can be categorized as catecholamines or non-catecholamines. Catecholamines like epinephrine cannot be used orally and have a short half-life, while non-catecholamines like ephedrine can be used orally and have a longer half-life. Examples of adrenergic drugs include pressor agents, cardiac stimulants, bronchodilators, and CNS stimulants. These drugs act through alpha, beta-1, and beta-2 receptors and are metabolized by monoamine oxidase and catechol-O-methyltransferase. Common adrenergic drugs and their uses include epinephrine for anaph
This document summarizes sympathomimetics and adrenergic transmission. It discusses the endogenous catecholamines norepinephrine, epinephrine, and dopamine, their synthesis, storage, release, reuptake, and metabolism. It describes the mechanisms of action of adrenergic drugs including direct and indirect sympathomimetics. The actions of catecholamines on various organs like the heart, blood vessels, lungs are explained. The document also covers adrenergic receptors, uses of sympathomimetics, adverse effects, contraindications, and sympatolytics.
This document summarizes the classification, mechanisms of action, pharmacokinetics, and clinical uses of α-adrenergic receptor antagonists (α-blockers). It discusses non-selective α-blockers that block both α1 and α2 receptors like phentolamine and phenoxybenzamine, as well as selective α1-blockers like prazosin, doxazosin, tamsulosin, and selective α2-blockers like yohimbine. The major uses of α-blockers include treatment of pheochromocytoma, hypertension, peripheral vascular disease, benign prostatic hyperplasia, migraine, and congestive heart failure. Common side effects include hypotension
This document discusses drugs that act on the autonomic nervous system. It covers neurotransmitters in the somatic and autonomic nervous systems like acetylcholine and catecholamines. It then categorizes and describes drugs that act on the sympathetic and parasympathetic nervous systems, including sympathomimetics, sympathomolytics, parasympathomimetics, and parasympatholytics. Specific drugs are discussed in detail including their mechanisms, uses, doses, and side effects.
This document discusses the adrenergic system and adrenergic drugs. It begins by describing the natural and synthetic catecholamines and non-catecholamines. It then discusses the biosynthesis, storage, release, reuptake, and metabolism of catecholamines. The document describes the different types of alpha and beta adrenergic receptors, their molecular effects, locations, and clinical effects. Specific catecholamines like adrenaline, noradrenaline, dopamine, and isoprenaline are discussed in detail regarding their actions, uses, and adverse effects. The therapeutic classifications and uses of various adrenergic drugs are provided.
Adrenergic agonist agents can be categorized as catecholamines or non-catecholamines. Catecholamines like epinephrine and norepinephrine cannot be used orally due to their short half-life and inability to cross the blood-brain barrier, while non-catecholamines like ephedrine can be used orally and cross the BBB due to their longer half-life. These agents act on alpha and beta adrenergic receptors and are used clinically as pressor agents, cardiac stimulants, bronchodilators, and more. Common adverse effects include anxiety, headache, and arrhythmias.
This presentation contains drugs which blocks the adrenergic system e.g receptor blockers like alpha and beta receptor antagonists, adrenergic neuron blocking agents in details.various animated pictures are also included to make the presentation interesting as well as i have used various diagrams and tables to have better understanding of the topic. Thank you.
This document discusses adrenergic receptors and modulators. It describes the sympathetic nervous system and neurotransmitters like norepinephrine, epinephrine, and dopamine. Norepinephrine is stored in synaptic vesicles and released via calcium-dependent fusion. Release can be modulated by prejunctional autoreceptors and heteroreceptors. There are alpha and beta adrenergic receptors which are G-protein coupled and have various effects. Drugs can affect receptors as agonists or antagonists and are used to treat conditions like hypertension and heart failure.
Adrenergic antagonists alpha and beta blockersZulcaif Ahmad
The document discusses various types of adrenergic receptor antagonists including alpha blockers like prazosin and terazosin which are used to treat hypertension and benign prostatic hyperplasia, as well as non-selective antagonists like phentolamine and beta blockers like propranolol which are used to treat conditions like hypertension, angina, and arrhythmias. The mechanisms, classifications, clinical uses and side effects of these different adrenergic antagonists are explained in detail across multiple pages.
Antiadrenergic drugs, also known as alpha blockers or alpha antagonists, work by blocking the effects of adrenaline and other related drugs at receptor sites. They occupy both alpha-1 and alpha-2 adrenergic receptors without activating them. Clinically, they are used to modify the responses of endogenous catecholamines like adrenaline and noradrenaline in both physiological and pathophysiological conditions. Common uses include treating pheochromocytoma, hypertension, Raynaud's disease, and benign prostatic hyperplasia. Individual drugs vary in their selectivity and duration of action at different receptor subtypes. Side effects may include postural hypotension, nasal congestion, and inhibition of ejac
The document discusses drugs that affect the autonomic nervous system, including adrenergic agents that stimulate the sympathetic nervous system and adrenergic blocking agents that inhibit sympathetic stimulation. It describes the locations and functions of alpha-1, alpha-2, and beta-1/2 receptors, examples of adrenergic drugs, their mechanisms of action and therapeutic uses, side effects, and nursing considerations.
The document discusses adrenergic drugs and their mechanisms of action. It notes that some adrenergic drugs act directly on adrenergic receptors to activate them, while others block receptor action. It provides tables listing examples of direct-acting, indirect-acting, and mixed-action adrenergic agonists. The document then discusses specific adrenergic drugs in more detail, including epinephrine, norepinephrine, isoproterenol, dopamine, dobutamine, oxymetazoline, phenylephrine, methoxamine, and clonidine. It explains their structures, receptor selectivities, and physiological effects.
This document discusses adrenergic agonists and antagonists. It begins by classifying adrenergic agonists as direct acting, mixed acting, or indirect acting. It then discusses specific alpha-1, alpha-2, beta-1, and beta-2 adrenergic receptor agonists like phenylephrine, clonidine, dobutamine, and terbutaline. It details their mechanisms of action and clinical indications. The document concludes by discussing classes of adrenergic antagonists including alpha receptor antagonists, beta receptor antagonists, and specific drugs like propranolol, prazocin, and yohimbine.
The document discusses adrenoceptor agonists and antagonists. It begins by providing an overview of the sympathetic nervous system and drugs that act on it. It then describes direct-acting sympathomimetic drugs that mimic norepinephrine and epinephrine by acting on alpha and beta receptors. Various agonists are discussed in depth, including their mechanisms of action, effects, uses, and adverse reactions. The document also covers adrenoceptor antagonists that block alpha and beta receptors, describing examples like prazosin and propranolol along with their clinical applications.
This document discusses non-catecholamine sympathomimetic drugs. It describes their general properties, classification based on receptor selectivity, and examples like ephedrine, pseudoephedrine, amphetamine, and tyramine. It covers the pharmacokinetics, pharmacodynamics, therapeutic uses, adverse effects and toxicity of these important non-catecholamine sympathomimetic drugs.
This document summarizes adrenergic agonists and antagonists. It describes the synthesis and metabolism of catecholamines like dopamine, norepinephrine, and epinephrine. It also discusses the different adrenergic receptor types (alpha and beta), their locations and functions. Various adrenergic drugs are classified and their mechanisms, effects, uses, and adverse effects outlined, including epinephrine, norepinephrine, dopamine, dobutamine, dopexamine, fenoldopam, phenylephrine, clonidine and others.
1. Prazosin is a potent and selective α1 adrenergic receptor blocker used to treat hypertension. It has a first-dose phenomenon that can cause severe hypotension, so the initial dose should be small.
2. Beta blockers block the effects of sympathetic stimulation by competitively blocking beta receptors. They are used to treat hypertension, angina, migraines, hyperthyroidism and other conditions. Common side effects include bradycardia, heart block, bronchospasm and hypoglycemia.
3. Drug interactions can occur between beta blockers and calcium channel blockers, local anesthetics, or bile acid sequestering resins which can affect absorption of the beta blockers
This document summarizes adrenergic agents and adrenergic-blocking agents. It describes how adrenergic agents mimic the effects of the sympathetic nervous system by stimulating alpha-adrenergic and beta-adrenergic receptors located throughout the body. It also describes how adrenergic-blocking agents, also called sympatholytics, inhibit the effects of the sympathetic nervous system by blocking these same receptors. Examples of different types of adrenergic and adrenergic-blocking agents are provided along with their therapeutic uses and important monitoring parameters.
This document discusses sympathomimetic drugs and adrenergic agonists. It describes how sympathomimetics mimic the effects of sympathetic nerve stimulation by acting on adrenergic receptors. It classifies adrenergic agonists as catecholamines or non-catecholamines and discusses their differences. It also summarizes the endogenous catecholamines, their synthesis, storage, and release. Additionally, it provides details on adrenergic receptors and the therapeutic uses, pharmacological actions, and side effects of various adrenergic drugs including epinephrine, dopamine, isoproterenol, dobutamine, ephedrine, and mephenteramine.
This document discusses various alpha and beta receptor antagonists. It provides details on their mechanisms of action, pharmacokinetics, clinical uses and side effects. Regarding alpha antagonists, it describes how they bind to alpha receptors to block catecholamine and sympathomimetic action. It also explains the differences between selective and non-selective alpha1 and alpha2 antagonists. For beta antagonists, it outlines their competitive inhibition of beta receptors and categorizes drugs as non-selective or cardioselective. The document discusses cardiovascular, respiratory, metabolic and other effects of both classes of drugs.
These are the drugs which antagonize the receptor action of adrenaline and related drugs.
These drugs act by blocking a and/or ß-adrenergic receptors.
α-blockers
PRAZOSIN is a competitive antagonist effective in the management of hypertension. Similar drugs with longer half-lives (e.g. doxazosin, terazosin).
β-blockers
Heart - Decrease heart rate, force of contraction and cardiac output.
Blood Pressure - Decrease in blood pressure (blockage).
Respiratory System – bronchoconstriction.
Eye – Beta-blocking agents reduce intraocular pressure, especially in glaucoma. The mechanism usually reported is decreased aqueous humor production.
Metabolic - Increase LDL and decrease HDL.
Uterus - Relaxation of uterus.
Local anaesthetic - Propranolol has some local anaesthetic action
This document discusses sympathomimetic drugs, which mimic the actions of epinephrine and norepinephrine. It describes the sympathetic and parasympathetic nervous systems, defines sympathomimetic drugs, and classifies them based on their mechanisms of action. The document also discusses the synthesis, storage, release, reuptake, and metabolism of catecholamines. It describes adrenergic receptors, where they are located, and provides examples of drugs that act on different receptor types. The actions and uses of epinephrine, norepinephrine, and dopamine are explained. Therapeutic classifications and examples of sympathomimetic drugs are also provided.
Adrenergic agonists can be categorized as catecholamines or non-catecholamines. Catecholamines like epinephrine cannot be used orally and have a short half-life, while non-catecholamines like ephedrine can be used orally and have a longer half-life. Examples of adrenergic drugs include pressor agents, cardiac stimulants, bronchodilators, and CNS stimulants. These drugs act through alpha, beta-1, and beta-2 receptors and are metabolized by monoamine oxidase and catechol-O-methyltransferase. Common adrenergic drugs and their uses include epinephrine for anaph
This document summarizes sympathomimetics and adrenergic transmission. It discusses the endogenous catecholamines norepinephrine, epinephrine, and dopamine, their synthesis, storage, release, reuptake, and metabolism. It describes the mechanisms of action of adrenergic drugs including direct and indirect sympathomimetics. The actions of catecholamines on various organs like the heart, blood vessels, lungs are explained. The document also covers adrenergic receptors, uses of sympathomimetics, adverse effects, contraindications, and sympatolytics.
This document summarizes the classification, mechanisms of action, pharmacokinetics, and clinical uses of α-adrenergic receptor antagonists (α-blockers). It discusses non-selective α-blockers that block both α1 and α2 receptors like phentolamine and phenoxybenzamine, as well as selective α1-blockers like prazosin, doxazosin, tamsulosin, and selective α2-blockers like yohimbine. The major uses of α-blockers include treatment of pheochromocytoma, hypertension, peripheral vascular disease, benign prostatic hyperplasia, migraine, and congestive heart failure. Common side effects include hypotension
This document discusses drugs that act on the autonomic nervous system. It covers neurotransmitters in the somatic and autonomic nervous systems like acetylcholine and catecholamines. It then categorizes and describes drugs that act on the sympathetic and parasympathetic nervous systems, including sympathomimetics, sympathomolytics, parasympathomimetics, and parasympatholytics. Specific drugs are discussed in detail including their mechanisms, uses, doses, and side effects.
This document discusses the adrenergic system and adrenergic drugs. It begins by describing the natural and synthetic catecholamines and non-catecholamines. It then discusses the biosynthesis, storage, release, reuptake, and metabolism of catecholamines. The document describes the different types of alpha and beta adrenergic receptors, their molecular effects, locations, and clinical effects. Specific catecholamines like adrenaline, noradrenaline, dopamine, and isoprenaline are discussed in detail regarding their actions, uses, and adverse effects. The therapeutic classifications and uses of various adrenergic drugs are provided.
This document discusses various classes of antihypertensive agents used to treat hypertension. It defines hypertension and describes the renin-angiotensin-aldosterone system which is important in regulating blood pressure. Common classes of antihypertensive agents discussed include diuretics, ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, alpha blockers, and central sympatholytics. Lifestyle modifications including weight loss, exercise, diet changes, and avoiding tobacco are also recommended for managing hypertension.
This document discusses various types of antihypertensive drugs including diuretics, renin-angiotensin system inhibitors, sympathetic inhibitors, calcium channel blockers, and vasodilators. It describes the mechanisms of action, pharmacological effects, drug interactions, and side effects of common antihypertensive drugs from each class such as hydrochlorothiazide, captopril, propranolol, nifedipine, and hydralazine. The document provides an overview of classifications, treatment approaches, and management of hypertension using different antihypertensive drug classes and combinations.
Pharmacology I Drugs acting on CVS
III B.Pharm, II Pharm D
Dr.Shivalinge Gowda KP Asso Professor and HOD
PES College of Pharmacy Bangalore-560050 Karnataka, India
shivalinge65@gmail.com
This document discusses various classes of antihypertensive drugs including their mechanisms of action and uses. It covers centrally acting drugs like clonidine and methyldopa which act on brain receptors to lower blood pressure. Ganglion blockers, adrenergic neuron blockers, alpha blockers, beta blockers, calcium channel blockers, ACE inhibitors, and angiotensin receptor antagonists are also discussed in terms of how they lower blood pressure through different mechanisms such as vasodilation, reduced cardiac output, or inhibition of the renin-angiotensin-aldosterone system. Common adverse drug reactions and clinical uses within each class are also summarized.
Sympathomimetic drugs mimic the actions of norepinephrine and epinephrine. They can act directly on alpha and beta adrenoceptors or indirectly by releasing norepinephrine from neurons. These drugs have many therapeutic uses including treating hypotension, cardiogenic shock, congestive heart failure, bronchial asthma, glaucoma, and more. The most important classes are epinephrine, norepinephrine, dopamine, dobutamine, and selective beta-2 agonists. They work by various mechanisms like increasing cardiac output, relaxing bronchioles, and constricting blood vessels.
About pharmacological classification of sympathetic nervus system both sympathomimetics and sympatholytics drug and all about his pharmacokinetics and pharmacodynamics action on body
1. Hypertension, or high blood pressure, requires treatment to prevent damage to blood vessels and organs like the heart, brain and kidneys.
2. There are several classes of antihypertensive agents that work through different mechanisms such as reducing sympathetic nervous system activity, blocking adrenoreceptors, vasodilation, and inhibiting the renin-angiotensin system.
3. Common antihypertensive drug classes discussed include ACE inhibitors, angiotensin II receptor blockers, beta blockers, calcium channel blockers, diuretics, and vasodilators. The appropriate treatment is selected based on the severity of the patient's high blood pressure.
This document discusses various classes of antihypertensive drugs including: diuretics (thiazide, loop, potassium-sparing), ACE inhibitors, ARBs, calcium channel blockers, beta blockers, alpha blockers, vasodilators, and central acting drugs. It provides details on mechanisms of action, examples within each class, their uses, and common side effects in treating hypertension. The renin-angiotensin-aldosterone system and how different drug classes target it at different levels is also explained.
Sympathomimetic drugs act on adrenergic receptors to mimic the effects of the sympathetic nervous system. Noradrenaline is the major neurotransmitter released by postganglionic sympathetic neurons. Catecholamines such as adrenaline, noradrenaline, and dopamine can be synthesized naturally or synthetically. They are released from neurons via exocytosis and cleared via reuptake or metabolism.
Adrenergic drugs include direct-acting sympathomimetics that activate receptors directly, indirect drugs that promote neurotransmitter release, and mixed drugs. Their effects are mediated via alpha and beta receptors. Common therapeutic uses include treating anaphylaxis, asthma, cardiac issues, and bleeding. Side effects can
Basic must know things about Anti Hypertensive drugs including the recent JNC-8 classification and protocols for treating Hypertension with various co-morbid condition.
Basic must know things about Anti-Hypertensives including the latest JNC-8 Classification and protocol for managing hypertension in various co-morbid conditions.
The document discusses adrenergic drugs and their mechanisms and uses. It describes how the sympathetic nervous system activates the fight or flight response through neurotransmitters like epinephrine and norepinephrine. It then covers different classes of adrenergic drugs including sympathomimetics that mimic sympathetic stimulation, vasopressors that constrict blood vessels, bronchodilators for asthma, and anorectics formerly used for weight loss. Specific drugs discussed include epinephrine, dopamine, dobutamine, ephedrine, amphetamines, and selective beta-2 agonists. A variety of conditions treated and contraindications are provided.
Beta receptors are G protein-coupled receptors that increase or decrease intracellular cAMP. Propranolol is a non-selective beta blocker that is well absorbed orally and metabolized in the liver. It decreases heart rate and force of contraction, has membrane stabilizing effects, and reduces the influence of norepinephrine on the heart. Propranolol blocks vasodilation, decreases blood pressure over time, and reduces norepinephrine release. It can also cause sedation, suppress anxiety, alter plasma lipids and carbohydrate tolerance, and worsen asthma.
This document provides an overview of sympathomimetic drugs, also known as adrenergic drugs. It defines them as drugs that have actions similar to adrenaline or sympathetic stimulation. It classifies them as direct, indirect, or mixed sympathomimetics and discusses examples of each. It then describes their pharmacological actions in detail, focusing on their effects on the cardiovascular system, respiration, eyes, gastrointestinal tract, bladder, uterus, skeletal muscle, central nervous system, and metabolism. Specific drugs discussed include adrenaline, noradrenaline, isoprenaline, dopamine, dobutamine, and phenylephrine. Therapeutic uses and adverse effects are also summarized.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
2. Adrenergic systems
• Also called sympathetic system ,
• catecholamine's system
• Sympathomimetic drugs
• Adrenergic agonist
• Adrenoreceptor agonist
• Sympathetic transmission are catecholamine in
nature and it includes – adrenaline , nor-
adrenaline , and dopamine secretion.
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4. SYNTHESIS , STORAGE ,RELEASE AND UPTAKE OF
ADRENALINE
All catecholamine are synthesized from amino acid
Phenylalanine in liver then hydrolyzed to tyrosine at end
of nerve.
• Methylation of Nor-adrenaline --adrenaline are
synthesized .
• Tyrosine hydroxylase is rate limiting enzyme and it
inhibited from METYROSINE.
१२/०२/२० 4
7. Action Potential
Na+
Effect of chronic b-receptor blockade:
Receptor up-regulation
H+
Effector organ
Tyrosine
Tyrosine
Dopamine
DA
NE
Uptake
1NE
NENENE
NE
8. • STORAGE –
• Noradrenalin stored in synaptic vesicles or granules within
the sympathetic nerve ending. On methylation in cytoplasm
NE convert into adrenaline in adrenal medulla.
• Release – CAs release out by nerve impulse with
exocytosis and indirectly by amines pumps.
• Uptake of CA s – Recaptured of CA from S.Junction by
two steps through nerve ending –
• 1) Axonal uptake –
Amine pump works to recaptured the NA and Adr from
synaptic junction. NET (amine pump) present at neuronal
membrane transport NA coupled with Na ion. This called
uptake -1. This uptake inhibited by cocaine, desipiramine,
guanathidine and many H1-antihistaminic drugs.१२/०२/२० 8
9. 2) Granular uptake -Intracellular amino pump which transport
CA from cytoplasm to within granules. Vascular monoamino
transport (VMAT) exchange with H+ ion which recaptured the NA
from axoplasm to granules or vesicles. This pump inhibited by
Resarpine as irreversibly and act
depleted the CA.
१२/०२/२० 9
H+
Uptake
Na ion exchange
Uptake 1
Axoplasm
Note-Uptake 2- is extra
neuronal uptake which take
place in cells and inhibited by
corticosterone
10. Metabolism
• CAs metabolized by Mono-amino oxidase (MAO) at site of
axonal part and in periphery like liver, blood and tissues,
metabolized by COMT (catechol-o- methyl transferase)
enzymes.
Adrenaline - -3,4 dihydroxy NE
mandelilic acid
Vanillylmandelic acid(VMA)
Glucoronide or sulphate conjugation
१२/०२/२० 10
COMT
MAO
11. Receptors α, β
• Adrenergic receptors act on α and β through G-
Protein coupled receptor which function primarily
by increase decreasing the intracellular function.
• Alpha (α) (1 , 2 )
• Beta (β)(1, 2 , 3)
• α 1 –
• Blood vessels- contraction
• Eye –mydriatics
• Prostate / urethera- decrease
• α 2- Pre-synaptic as well as post syneptic nerve
ending.
१२/०२/२०
Main location
11
14. Classification of Adrenergic drugs
• By mode of action
Direct acting- CA and Non CA
-Indirect acting- Tyramine, amphetamine, cocaine,
ephedrine, TCA
• By chemistry
– Catecholamines (CA)
– Non-catecholamines
• By selectivity (to types of receptor)
Direct acting
• classified by alpha, beta receptor subtypes
• a 1 -selective, a 2 -selective, nonselective
• b 1 -selective, b 2 -selective , nonselectiv
१२/०२/२० 14
15. Difference between CA and non CA
१२/०२/२० 15
Catecholamines
– Cannot be given orally
– Short half-life, short duration
– Not cross blood-brain barrier (BBB)
Reasons: due to having catachol group
– Rapid destruction by MAO and COMT
– MAO, COMT locate at gut wall, liver
– High polarity
16. • Indirect acting sympathomimetic drugs
• tyramine
• amphetamine
• Mixed action sympathomimetics-
• Ephedrine
• Dopamine
१२/०२/२०
Classification based on
therapeutic action
see in BOOK –page no. 88
16
18. PHARMACOLOGICAL ACTION
• In periphery adrenaline acts on alpha and beta
receptors of different tissues and organs . Some
important actions are –
• On Heart ;- Adrenaline increase the heart rate , by
acting on Beta-1 receptor and its result
Systole is shortened then diastole
Cardiac output and oxygen
consumption markedly increased.
Increase in atomicity, excitability which cause
cardiac arrhythmia.
१२/०२/२०
+ve chronotropic
+ve ionotropic
+dromotropic
18
19. Action on heart
१२/०२/२० 19
• Biphasic
• Small dose – Fall in BP – due to beta receptor stimulation
• High dose – Rise in BP – due to alpha receptor
stimulation
alpha Beta
20. • Blood vessels – Vasoconstrictor(alpha-1) as well as
vasodilator (bata-2), depends on the action of
drugs. Action is most marked on arterioles due to
alpha-1, and larger arteries and veins due to beta-
2.
• BP- Noradrenaline causes vasoconstriction (alpha-1),
beta-1 receptor is responsible for increased in BP.
Result- increased BP, but it cause bradycardia- but adr
caused- tachycardia
• Respiratory systems – Adr and isoprenaline and NA acts
on beta-2 of bronchus results dilation of bronchial smooth
muscles . NA Potent bronchodilator (indirectly)but short
duration of action. Reduce secretions release mucosal
congestion by vasoconstriction.
१२/०२/२० 20
21. • Eye- Mydriatics occurs due to relaxation of radial
muscles of iris (alpha-1) .
• GIT – Gut relaxation occurs through activation of both
Alpha and Beta – receptors. Peristalsis and sphincter are
reduced but is not such effective, so no any clinical
importance .
• Bladder –Detrusor is relaxed (beta-2) and trigone is constrict
(alpha-1) – resulting hinder micturition.
• Uterus –Contraction through alpha while relaxation
through beta receptors .
• Skeleton muscles –Contraction of muscles, tension developed
in muscles fibers which may cause tremor mediated by Beta –
receptors.
१२/०२/२० 21
22. • CNS – Clinical dose of adrenaline produced NO any
marked effects on CNS, because of poor penetration of
BBB. When injected in brain it produced excitation
followed by depression .
Activation of alpha -2 receptors of brainstem results in decrease in
sympathetic outflow and cause bradycardia.
• Metabolic – Increase blood glucose level by increasing
the cAMP in liver cell and stimulating glycogenolysis
through Beta -2 receptors . Reduction of insulin and
Glycogenolysis may cause increase glucose level in blood.
• Glands – Decrease the secretion of glands.
१२/०२/२० 22
23. Pharmacokinetics
Adrenaline / CA are not suitable for oral route
due to different enzymes metabolism present in
GIT and liver like COMT and MAO.
Absorption is more rapid after intramuscular
injection but sometimes given as IV.
In anaphylactic it given as IV, due to poor
absorption.
catecholamine does not cross BBB.
No neuronal uptake like CA
१२/०२/२० 23
25. Contradicted
• In hypertension condition
• Hyperthyroid
• Angina pectoris
• With anesthesia like halothene
• Adrenaline contradicted in GTN , angina ,
CCF , arrhythmias
१२/०२/२० 25
26. Adrenergic USES
• Nocturnal enuresis in
children and urinary
incontinence
• Uterine relaxant
• Insulin hypoglycaemia
• Hyperkinetic children
• Narcolepsy
• Obesity
१२/०२/२०
VASCULAR USES
• Hypotensive state
• Along with local anaesthetics
• Control of local bleeding
• Nasal decongestant
CARDIAC USES
• Cardiac arrest
• Partial or complete A-V block
• Congestive heart failure (CHF)
• Bronchial asthma
• Allergic disorders
• Mydriatic 26
27. • In cardiac arrest and heart block ,the drug of choice is
adrenaline (0.3-0.5 ml of 1;1000 solution) .
• Used in anaphylactic shock
• In acute bronchial asthma (beta-2 agonist)
• Inhibition of premature labour (salbutamol).
• In bronchial asthma ,
• Allergic
• for mydriatic ,
• Narcolepsy
• Obesity ,
• uterine relaxant , in hypoglycemia .
१२/०२/२० 27
28. Dopamine
• It is central neurotransmitter and it acts on dopaminergic and adrenergic
receptors .
• It is catecholamine, present in CNS as well as periphery, transported in vesicles
and blocked by reserpine .
• MOA- it acts on centrally present dopaminergic receptors D1, D2 as well as
beta-1, alpha-1 receptors (with increasing dose).
• PHARMACOKINETICS-
• Show High 1st pass effect. It metabolised by both MAO and COMT.
• Thus it is ineffective when administered orally. Most sensitive to IV at low
dose.
• Prodrug of dopamine is ineffective to metabolized enzyme and cross BBB.
•
१२/०२/२० 28
29. • Pharmacological effects
• Heart –dopamine has direct action on beta -1 receptor
and act like positive chronotropic and inotropic and
increase HR
• Blood vessels – act as vasoconstrictor (alpha-1) –increase BP on
high dose .
• Renal – INCREASING g.f.r. and Na excretion. Activation of
D1 receptors in several vascular beds, of kidney which
leads to vasodilation. Diminished Na+ reabsorption by
the proximal tubular cells cause natriuretic (beta-1)
• CNS-There is no effect on CNS , due to DA not cross BBB .
• Therapeutic use – In treatment of septic shock specially with oliguria
patient's (dose is >2-10 mcg/body wt.) .In renal dysfunction and cardiac arrest
, CHF
१२/०२/२० 29
30. Amphetamine
• Non-catacholamine synthetic and sympathomimetic
drugs . It having both central and peripheral effect.
• MOA- It having indirectly stimulate adrenergic receptor
by increasing release of catecholamine including 5-HT .
P’COLOGICAL ACTION-
• CNS – Crosses BBB and act potent CNS stimulant ,
physical activity, alertness ,euphoria , reduces sleep
,reduces hunger and appetite. It also increase initiative
and self-confidence and increase capacity to work.
• Respiration – stimulate respiratory Centre
• Heart – low dose not effect but high dose cause positive
chronotropic. १२/०२/२०
31. • p’kinetic – orally effective for long duration .
Crosses BBB. metabolized by liver enzymes.
Excreted through acidic urine easily.
• Therapeutic Use – In CNS stimulant
• In ADHD (attention disorder hyperkinetic
deficiency) in children.- drug-Methylphenidate
• In obesity.
• Increase Attention spasm
• Reduce sleep (Drug of choice- medafinil)
• Epileptics and parkinsonism .
• Week anticonvulsants, analgesic antiemetic, and acta
as synergetic to above drugs.१२/०२/२० 31
32. It is one of the drug which used in Dope Test
• ADR-
• Amphetamine come under shedule-2
• These are drug of abuse and are producing
psychological dependency . (DOPING)
• Higher dose causes confusion delirium, acute
psychosis , coma and death also.
१२/०२/२०
Thank u
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