This document discusses the pharmacology of receptors, including the main types of receptors, how they function through secondary messengers, and how they can be regulated. It covers ligand-gated ion channels, G protein-coupled receptors, and transcription factors. Receptor regulation and drug-receptor interactions are also explained. The document notes how receptor malfunctions can cause diseases and the significance of receptor subtypes for developing subtype-selective drugs.
The document summarizes the main types of protein targets for drug action in mammalian cells. It discusses four main types:
1) Receptors, which are membrane proteins that sense chemical messengers like hormones and transmitters. They include ligand-gated ion channels, G-protein coupled receptors, kinase-linked receptors, and nuclear receptors.
2) Ion channels, which are membrane proteins that allow ions to pass through. They include ligand-gated ion channels and voltage-gated channels.
3) Enzymes, which are targets of drugs that act as competitive or irreversible inhibitors.
4) Carrier molecules called transporters, which transport ions and molecules across cell membranes using carrier proteins
Receptors are proteins that bind to specific molecules called ligands. There are two main types of receptors: intracellular receptors located inside the cell, and cell surface receptors located in the plasma membrane. Receptor function involves binding of a ligand, which causes a conformational change in the receptor and transmission of a signal. Some important receptor types include ligand-gated ion channels, G protein-coupled receptors, and enzyme-linked receptors such as receptor tyrosine kinases. Mutations in receptor tyrosine kinases can cause developmental disorders and cancers due to effects on cell growth, differentiation, and apoptosis.
This document discusses different types of receptors and how they transmit signals. It describes two main domains of receptors - a recognition domain that binds hormones and a coupling domain that generates an intracellular signal. It also discusses three types of cell surface receptors - ion channel receptors, transmembrane receptors, and receptors that are kinases or bind kinases. Steroid hormones can directly activate genes by diffusing into the cell and binding intracellular receptors, which then bind DNA and activate transcription.
Polymorphism affecting drug metabolismDeepak Kumar
Genetic polymorphisms can affect how individuals metabolize and respond to drugs. Variations in genes encoding drug-metabolizing enzymes like CYP450 isoforms can result in poor, intermediate, extensive, or ultra-rapid metabolizer phenotypes. This impacts how effectively an individual metabolizes and eliminates drugs from the body. The effects of inhibitors and inducers on drug metabolism also differ depending on a person's metabolizer phenotype. Understanding these genetic factors is important for predicting drug responses and interactions between a drug and other substances in an individual.
G protein coupled receptors and their Signaling MechanismFarazaJaved
G protein-coupled receptors (GPCRs) are a large family of receptors that span cell membranes and activate intracellular signaling pathways in response to extracellular stimuli. They are activated by a wide range of ligands including light, hormones, and neurotransmitters. Upon ligand binding, GPCRs activate heterotrimeric G proteins, which then initiate intracellular signaling cascades. The three main G protein families - Gs, Gi, and Gq - activate or inhibit different downstream effector enzymes to elicit a cellular response. Dysregulation of GPCRs and their associated signaling pathways can lead to various diseases.
Classification of receptors family by vivek sharmaAnimatedWorld
Definition- Receptor are the biologic molecule to which drug bind and produces a measurable response.
So, enzyme and structural proteins can be considerd to be pharmacologic receptors.
Majorly receptor are of 4 types and the molecule or a drug interact to receptor to give response often called as ligand.
The type of receptor a ligand will bind is depend on the nature of ligand.
Hydrophilliic ligand binds to the receptor found on the cell surface.
Hydrophobic ligand can enter the cell membrane to intract the receptor present on inside the cells.
Classification of Receptors
A. Cell surface receptor
Ligand-gated Ion Channel
G Protein Coupled Receptor
Enzyme linked Receptor
B. Intracellular Receptor
Nuclear Receptor
The document discusses receptor desensitization, which is the decrease in response of cells to agonists after continuous stimulation. It can occur via two types: homologous, mediated by the same receptor; or heterologous, mediated by a different receptor. Factors that can cause desensitization include changes to receptors, loss of receptors, exhaustion of mediators, increased drug metabolism, and physiological adaptation. The mechanism involves phosphorylation of receptors and binding of arrestins, which uncouple the receptor from G proteins and promote internalization. β-arrestins play a key role in desensitization and can also translocate to the nucleus to influence transcription.
The document summarizes the main types of protein targets for drug action in mammalian cells. It discusses four main types:
1) Receptors, which are membrane proteins that sense chemical messengers like hormones and transmitters. They include ligand-gated ion channels, G-protein coupled receptors, kinase-linked receptors, and nuclear receptors.
2) Ion channels, which are membrane proteins that allow ions to pass through. They include ligand-gated ion channels and voltage-gated channels.
3) Enzymes, which are targets of drugs that act as competitive or irreversible inhibitors.
4) Carrier molecules called transporters, which transport ions and molecules across cell membranes using carrier proteins
Receptors are proteins that bind to specific molecules called ligands. There are two main types of receptors: intracellular receptors located inside the cell, and cell surface receptors located in the plasma membrane. Receptor function involves binding of a ligand, which causes a conformational change in the receptor and transmission of a signal. Some important receptor types include ligand-gated ion channels, G protein-coupled receptors, and enzyme-linked receptors such as receptor tyrosine kinases. Mutations in receptor tyrosine kinases can cause developmental disorders and cancers due to effects on cell growth, differentiation, and apoptosis.
This document discusses different types of receptors and how they transmit signals. It describes two main domains of receptors - a recognition domain that binds hormones and a coupling domain that generates an intracellular signal. It also discusses three types of cell surface receptors - ion channel receptors, transmembrane receptors, and receptors that are kinases or bind kinases. Steroid hormones can directly activate genes by diffusing into the cell and binding intracellular receptors, which then bind DNA and activate transcription.
Polymorphism affecting drug metabolismDeepak Kumar
Genetic polymorphisms can affect how individuals metabolize and respond to drugs. Variations in genes encoding drug-metabolizing enzymes like CYP450 isoforms can result in poor, intermediate, extensive, or ultra-rapid metabolizer phenotypes. This impacts how effectively an individual metabolizes and eliminates drugs from the body. The effects of inhibitors and inducers on drug metabolism also differ depending on a person's metabolizer phenotype. Understanding these genetic factors is important for predicting drug responses and interactions between a drug and other substances in an individual.
G protein coupled receptors and their Signaling MechanismFarazaJaved
G protein-coupled receptors (GPCRs) are a large family of receptors that span cell membranes and activate intracellular signaling pathways in response to extracellular stimuli. They are activated by a wide range of ligands including light, hormones, and neurotransmitters. Upon ligand binding, GPCRs activate heterotrimeric G proteins, which then initiate intracellular signaling cascades. The three main G protein families - Gs, Gi, and Gq - activate or inhibit different downstream effector enzymes to elicit a cellular response. Dysregulation of GPCRs and their associated signaling pathways can lead to various diseases.
Classification of receptors family by vivek sharmaAnimatedWorld
Definition- Receptor are the biologic molecule to which drug bind and produces a measurable response.
So, enzyme and structural proteins can be considerd to be pharmacologic receptors.
Majorly receptor are of 4 types and the molecule or a drug interact to receptor to give response often called as ligand.
The type of receptor a ligand will bind is depend on the nature of ligand.
Hydrophilliic ligand binds to the receptor found on the cell surface.
Hydrophobic ligand can enter the cell membrane to intract the receptor present on inside the cells.
Classification of Receptors
A. Cell surface receptor
Ligand-gated Ion Channel
G Protein Coupled Receptor
Enzyme linked Receptor
B. Intracellular Receptor
Nuclear Receptor
The document discusses receptor desensitization, which is the decrease in response of cells to agonists after continuous stimulation. It can occur via two types: homologous, mediated by the same receptor; or heterologous, mediated by a different receptor. Factors that can cause desensitization include changes to receptors, loss of receptors, exhaustion of mediators, increased drug metabolism, and physiological adaptation. The mechanism involves phosphorylation of receptors and binding of arrestins, which uncouple the receptor from G proteins and promote internalization. β-arrestins play a key role in desensitization and can also translocate to the nucleus to influence transcription.
Neuropeptides are small protein-like molecules that neurons use to communicate with each other. They are responsible for many brain functions including analgesia, food intake, learning and memory, metabolism, and social behaviors. Some key neuropeptides discussed are Neuropeptide Y, which regulates appetite, and Tachykinins like Substance P which mediates pain. Arginine vasopressin regulates water balance and social behaviors through G protein-coupled receptors.
The JAK/STAT pathway involves cytokines binding to cell surface receptors which activates JAK kinases, leading to phosphorylation of STAT transcription factors. STAT dimers then enter the nucleus and regulate transcription of genes involved in processes like proliferation, differentiation, and survival. Disregulation of the JAK/STAT pathway contributes to diseases like leukemia, and JAK inhibitors have been developed for leukemia therapy.
Transmembrane ion channels are protein pores that regulate the passage of ions across cell membranes. There are two main types - voltage-gated ion channels, which open and close in response to changes in membrane potential, and ligand-gated ion channels, which open when certain chemical messengers bind to them. Key voltage-gated channels include sodium, calcium, and potassium channels. Major ligand-gated channels are nicotinic acetylcholine receptors, GABAA receptors, glutamate receptors, and ATP-sensitive potassium channels. The discovery and study of ion channels over time has provided crucial insights into nerve signaling and other cellular processes.
Ion channels, types and their importace in managment of diseasesFarazaJaved
This topic covers voltage gated type of ion channel, general structure and functioning of ion channels and involvement of different ion channel types in the pathogenesis as wella as a target for the development of various diseases.
G Protein–Coupled Receptors (GPCRs) are integral membrane proteins that are activated by extracellular signaling molecules and activate intracellular secondary messenger pathways. They have seven transmembrane domains and activate heterotrimeric G proteins upon ligand binding. The G protein then activates downstream effector enzymes like adenylyl cyclase, which generates secondary messengers like cAMP. These messengers go on to activate pathways that ultimately alter cell function. The beta-adrenergic receptor pathway is a key example, with epinephrine binding and cAMP production leading to protein kinase A activation. PKA then phosphorylates target proteins to produce effects like increased heart rate. GPCRs are major drug targets, and their deregulation
Cell death, also known as programmed cell death, occurs through various pathways including apoptosis, autophagy, and necrosis. Apoptosis, or programmed cell death, involves two main pathways - the intrinsic pathway which is triggered by cellular stress and the extrinsic pathway which is triggered by death ligands binding to cell surface death receptors. Both pathways activate caspases that break down cellular components leading to cell death. Autophagy is the natural and regulated mechanism by which cells degrade and recycle unnecessary or dysfunctional cellular components through the formation of autophagosomes and lysosomal degradation. Necrosis is unregulated cell death caused by external factors like infection, trauma or ischemia and results in the premature death of cells and tissue damage
MAPK Signaling pathway (Mitogen-activated protein kinase), how the pathway helps in regulation of mitosis, It's activation and inactivation inside the cell, roles of MAPK pathway in cancerous cell, different classes of MAP kinase in human
The MAPK pathway is a signal transduction pathway that responds to extracellular stimuli and regulates various cellular processes. It involves a phosphorylation cascade from MAPKKK to MAPKK to MAPK that ultimately regulates transcription factors and gene expression. Second messengers like cAMP, IP3, and calcium amplify extracellular signals and allow cross-talk between different pathways. The MAPK pathway controls processes like cell growth, division, survival, and metabolism.
Nitric oxide (NO) is an important signalling molecule in the body that regulates many physiological processes. It is synthesized by nitric oxide synthase enzymes from L-arginine and oxygen. NO signals through activation of soluble guanylate cyclase and production of cyclic GMP. It has diverse effects in the cardiovascular, immune, and nervous systems and is involved in processes like vasodilation, neurotransmission, and inflammation. Both insufficient and excessive NO production can contribute to disease.
Earl Wilbur Sutherland Jr. discovered cyclic AMP (cAMP) as a second messenger that allows hormones like epinephrine to trigger physiological responses in cells. cAMP is produced from ATP by adenylate cyclase in response to hormone binding and activates protein kinase A. Protein kinase A then phosphorylates other proteins to initiate downstream cellular effects. The actions of cAMP are terminated by phosphodiesterase breaking it down and by dephosphorylation of proteins. cAMP mediates many important processes like glycogen breakdown and gene transcription.
This document summarizes kinase receptors and nuclear receptors. Kinase receptors contain an extracellular ligand-binding domain connected by a transmembrane helix to an intracellular domain with kinase activity. They signal through phosphorylation cascades like MAPK. Nuclear receptors regulate gene transcription as ligand-activated transcription factors. They contain a ligand binding domain, DNA binding domain, and transcriptional regulation domain. Nuclear receptors form dimers and recruit cofactors to modify gene expression.
Cell surface receptors transmit signals from outside the cell via signal transduction pathways. Receptors are divided into classes including ion channel-linked and enzyme-linked receptors. Enzyme-linked receptors contain intrinsic enzyme activity or associate with intracellular enzymes. Upon ligand binding, a conformational change activates the enzyme, initiating signaling cascades. Tyrosine kinase receptors have intrinsic kinase activity that phosphorylates tyrosines, creating docking sites and activating downstream pathways such as MAPK cascades. Mutations in these receptors and associated kinases can cause cancers and developmental disorders.
The document discusses receptor tyrosine kinases (RTKs), a class of cell surface receptors that possess intrinsic tyrosine kinase activity. RTKs are activated through ligand binding and dimerization, which leads to autophosphorylation and downstream signaling. This signaling involves phosphorylation of proteins by RTKs and recruitment of adapter proteins, and results in cellular responses like cell division, differentiation, and motility. Common to all RTKs are an extracellular ligand-binding domain, a transmembrane domain, an intracellular tyrosine kinase domain, and regulatory domains.
Nuclear receptors are a family of transcription factors that bind small molecule ligands and regulate gene expression. They contain several domains including a DNA binding domain and ligand binding domain. Upon ligand binding, nuclear receptors undergo a conformational change and recruit coactivators or corepressors to activate or repress transcription. They are classified into three classes based on their localization and dimerization properties. Class II nuclear receptors like PPARs form heterodimers with RXR, bind lipids, and regulate metabolism. PPARγ agonists like glitazones bind PPARγ, activate gene transcription, and have antidiabetic effects like sensitizing tissues to insulin.
G protein-coupled receptors (GPCRs) are a large family of transmembrane receptors that sense molecules outside the cell and activate intracellular signal transduction pathways. They have seven transmembrane domains and transmit signals by coupling to heterotrimeric G proteins on the inner cell surface. When an agonist binds to a GPCR, it causes a conformational change that activates the G protein, starting intracellular signaling cascades through second messengers like cAMP or IP3. Approximately half of all drugs target GPCRs, making them an important drug discovery area.
Receptor types, mechanism, receptor pharmacology, drug receptor interactions, theories of receptor pharmacology, spare receptors and new concepts like biased agonism
Intrinsic and Extrinsic Pathway of ApoptosisAnantha Kumar
This document provides an overview of apoptosis (programmed cell death) at the cellular level. It discusses how apoptosis can be initiated through either the intrinsic or extrinsic pathway. The intrinsic pathway involves signals within the cell like mitochondrial membrane permeability, while the extrinsic pathway involves death receptors on the cell surface and their ligands. Key proteins and complexes involved in each pathway are caspase enzymes and the apoptosome. Research on apoptosis has increased understanding of diseases like cancer that involve deregulated cell proliferation and death.
The document discusses the principles of pharmacodynamics, which is the study of how drugs act on the body. It describes how drugs interact with receptors like G-protein coupled receptors, ion channels, and transmembrane receptors to exert their effects. The mechanisms of drug action include receptor binding and activation of downstream signaling pathways like the cAMP pathway or phospholipase C pathway. The document provides examples of how different receptors and signaling pathways influence various physiological processes in the body.
This document discusses pharmacodynamics and receptor interactions. It defines pharmacodynamics as the relationship between drug concentration at the receptor site and the resulting pharmacological response. It describes the four main receptor families - ligand-gated ion channels, G protein-coupled receptors, enzyme-linked receptors, and intracellular receptors. It also discusses receptor ligands, agonists, antagonists, affinity, efficacy, dose-response relationships, and therapeutic indices.
Neuropeptides are small protein-like molecules that neurons use to communicate with each other. They are responsible for many brain functions including analgesia, food intake, learning and memory, metabolism, and social behaviors. Some key neuropeptides discussed are Neuropeptide Y, which regulates appetite, and Tachykinins like Substance P which mediates pain. Arginine vasopressin regulates water balance and social behaviors through G protein-coupled receptors.
The JAK/STAT pathway involves cytokines binding to cell surface receptors which activates JAK kinases, leading to phosphorylation of STAT transcription factors. STAT dimers then enter the nucleus and regulate transcription of genes involved in processes like proliferation, differentiation, and survival. Disregulation of the JAK/STAT pathway contributes to diseases like leukemia, and JAK inhibitors have been developed for leukemia therapy.
Transmembrane ion channels are protein pores that regulate the passage of ions across cell membranes. There are two main types - voltage-gated ion channels, which open and close in response to changes in membrane potential, and ligand-gated ion channels, which open when certain chemical messengers bind to them. Key voltage-gated channels include sodium, calcium, and potassium channels. Major ligand-gated channels are nicotinic acetylcholine receptors, GABAA receptors, glutamate receptors, and ATP-sensitive potassium channels. The discovery and study of ion channels over time has provided crucial insights into nerve signaling and other cellular processes.
Ion channels, types and their importace in managment of diseasesFarazaJaved
This topic covers voltage gated type of ion channel, general structure and functioning of ion channels and involvement of different ion channel types in the pathogenesis as wella as a target for the development of various diseases.
G Protein–Coupled Receptors (GPCRs) are integral membrane proteins that are activated by extracellular signaling molecules and activate intracellular secondary messenger pathways. They have seven transmembrane domains and activate heterotrimeric G proteins upon ligand binding. The G protein then activates downstream effector enzymes like adenylyl cyclase, which generates secondary messengers like cAMP. These messengers go on to activate pathways that ultimately alter cell function. The beta-adrenergic receptor pathway is a key example, with epinephrine binding and cAMP production leading to protein kinase A activation. PKA then phosphorylates target proteins to produce effects like increased heart rate. GPCRs are major drug targets, and their deregulation
Cell death, also known as programmed cell death, occurs through various pathways including apoptosis, autophagy, and necrosis. Apoptosis, or programmed cell death, involves two main pathways - the intrinsic pathway which is triggered by cellular stress and the extrinsic pathway which is triggered by death ligands binding to cell surface death receptors. Both pathways activate caspases that break down cellular components leading to cell death. Autophagy is the natural and regulated mechanism by which cells degrade and recycle unnecessary or dysfunctional cellular components through the formation of autophagosomes and lysosomal degradation. Necrosis is unregulated cell death caused by external factors like infection, trauma or ischemia and results in the premature death of cells and tissue damage
MAPK Signaling pathway (Mitogen-activated protein kinase), how the pathway helps in regulation of mitosis, It's activation and inactivation inside the cell, roles of MAPK pathway in cancerous cell, different classes of MAP kinase in human
The MAPK pathway is a signal transduction pathway that responds to extracellular stimuli and regulates various cellular processes. It involves a phosphorylation cascade from MAPKKK to MAPKK to MAPK that ultimately regulates transcription factors and gene expression. Second messengers like cAMP, IP3, and calcium amplify extracellular signals and allow cross-talk between different pathways. The MAPK pathway controls processes like cell growth, division, survival, and metabolism.
Nitric oxide (NO) is an important signalling molecule in the body that regulates many physiological processes. It is synthesized by nitric oxide synthase enzymes from L-arginine and oxygen. NO signals through activation of soluble guanylate cyclase and production of cyclic GMP. It has diverse effects in the cardiovascular, immune, and nervous systems and is involved in processes like vasodilation, neurotransmission, and inflammation. Both insufficient and excessive NO production can contribute to disease.
Earl Wilbur Sutherland Jr. discovered cyclic AMP (cAMP) as a second messenger that allows hormones like epinephrine to trigger physiological responses in cells. cAMP is produced from ATP by adenylate cyclase in response to hormone binding and activates protein kinase A. Protein kinase A then phosphorylates other proteins to initiate downstream cellular effects. The actions of cAMP are terminated by phosphodiesterase breaking it down and by dephosphorylation of proteins. cAMP mediates many important processes like glycogen breakdown and gene transcription.
This document summarizes kinase receptors and nuclear receptors. Kinase receptors contain an extracellular ligand-binding domain connected by a transmembrane helix to an intracellular domain with kinase activity. They signal through phosphorylation cascades like MAPK. Nuclear receptors regulate gene transcription as ligand-activated transcription factors. They contain a ligand binding domain, DNA binding domain, and transcriptional regulation domain. Nuclear receptors form dimers and recruit cofactors to modify gene expression.
Cell surface receptors transmit signals from outside the cell via signal transduction pathways. Receptors are divided into classes including ion channel-linked and enzyme-linked receptors. Enzyme-linked receptors contain intrinsic enzyme activity or associate with intracellular enzymes. Upon ligand binding, a conformational change activates the enzyme, initiating signaling cascades. Tyrosine kinase receptors have intrinsic kinase activity that phosphorylates tyrosines, creating docking sites and activating downstream pathways such as MAPK cascades. Mutations in these receptors and associated kinases can cause cancers and developmental disorders.
The document discusses receptor tyrosine kinases (RTKs), a class of cell surface receptors that possess intrinsic tyrosine kinase activity. RTKs are activated through ligand binding and dimerization, which leads to autophosphorylation and downstream signaling. This signaling involves phosphorylation of proteins by RTKs and recruitment of adapter proteins, and results in cellular responses like cell division, differentiation, and motility. Common to all RTKs are an extracellular ligand-binding domain, a transmembrane domain, an intracellular tyrosine kinase domain, and regulatory domains.
Nuclear receptors are a family of transcription factors that bind small molecule ligands and regulate gene expression. They contain several domains including a DNA binding domain and ligand binding domain. Upon ligand binding, nuclear receptors undergo a conformational change and recruit coactivators or corepressors to activate or repress transcription. They are classified into three classes based on their localization and dimerization properties. Class II nuclear receptors like PPARs form heterodimers with RXR, bind lipids, and regulate metabolism. PPARγ agonists like glitazones bind PPARγ, activate gene transcription, and have antidiabetic effects like sensitizing tissues to insulin.
G protein-coupled receptors (GPCRs) are a large family of transmembrane receptors that sense molecules outside the cell and activate intracellular signal transduction pathways. They have seven transmembrane domains and transmit signals by coupling to heterotrimeric G proteins on the inner cell surface. When an agonist binds to a GPCR, it causes a conformational change that activates the G protein, starting intracellular signaling cascades through second messengers like cAMP or IP3. Approximately half of all drugs target GPCRs, making them an important drug discovery area.
Receptor types, mechanism, receptor pharmacology, drug receptor interactions, theories of receptor pharmacology, spare receptors and new concepts like biased agonism
Intrinsic and Extrinsic Pathway of ApoptosisAnantha Kumar
This document provides an overview of apoptosis (programmed cell death) at the cellular level. It discusses how apoptosis can be initiated through either the intrinsic or extrinsic pathway. The intrinsic pathway involves signals within the cell like mitochondrial membrane permeability, while the extrinsic pathway involves death receptors on the cell surface and their ligands. Key proteins and complexes involved in each pathway are caspase enzymes and the apoptosome. Research on apoptosis has increased understanding of diseases like cancer that involve deregulated cell proliferation and death.
The document discusses the principles of pharmacodynamics, which is the study of how drugs act on the body. It describes how drugs interact with receptors like G-protein coupled receptors, ion channels, and transmembrane receptors to exert their effects. The mechanisms of drug action include receptor binding and activation of downstream signaling pathways like the cAMP pathway or phospholipase C pathway. The document provides examples of how different receptors and signaling pathways influence various physiological processes in the body.
This document discusses pharmacodynamics and receptor interactions. It defines pharmacodynamics as the relationship between drug concentration at the receptor site and the resulting pharmacological response. It describes the four main receptor families - ligand-gated ion channels, G protein-coupled receptors, enzyme-linked receptors, and intracellular receptors. It also discusses receptor ligands, agonists, antagonists, affinity, efficacy, dose-response relationships, and therapeutic indices.
Drug Receptors intercaction and Drug antagonism : Dr Rahul Kunkulol's Power p...Rahul Kunkulol
1. The document discusses various types of drug receptors and receptor superfamilies including ligand-gated ion channels, G-protein coupled receptors, kinase-linked receptors, and nuclear receptors.
2. It describes the mechanisms of drug-receptor interactions and signal transduction pathways involving second messengers like cAMP, IP3, DAG, Ca2+, and nitric oxide.
3. The concepts of agonism, antagonism, partial agonism, and theories of drug-receptor binding like the two-state model are explained. Different types of antagonism like competitive and non-competitive are also summarized.
This document provides an overview of pharmacology concepts related to receptors and drug action. It defines key terms like agonists, antagonists, efficacy, and potency. It describes the four major families of pharmacologic receptors - ligand-gated ion channels, G protein-coupled receptors, enzyme-linked receptors, and intracellular receptors. Within each family it provides examples of receptors, the mechanism of drug action, and representative drugs. The document also distinguishes between different types of agonists, antagonists, and mechanisms of drug-receptor interactions.
The document discusses the mechanisms of drug action, which can generally be categorized into four types: enzymes, ion channels, transporters, and receptors. It provides examples for each category and describes how drugs can interact with these biomolecules to produce their effects. For receptors specifically, it defines terms like agonist, antagonist, partial agonist, and discusses different receptor families like G-protein coupled receptors and enzyme-linked receptors. It also touches on concepts like drug potency, efficacy, therapeutic index, synergistic and antagonistic drug interactions.
- Drug receptors, also known as drug targets, are cellular macromolecules or complexes that drugs interact with to elicit a cellular response and change cell function.
- There are various classifications of receptors including pharmacological, biochemical, molecular, anatomical, and GPCR classifications.
- The two main types of receptors are ligand-gated ion channels and G protein-coupled receptors. Ligand-gated ion channels allow ion flow through the cell membrane in response to ligand binding, while GPCRs signal via G proteins to activate intracellular effector mechanisms.
This document discusses theories of drug receptor interaction. It describes the occupation theory which states that pharmacological effect is proportional to the number of occupied receptors. It also discusses the rate theory, induced fit theory, macromolecular perturbation theory, activation-aggregation theory, and two-state model of receptor activation. Each theory provides a different perspective on how drugs interact with receptors and elicit biological responses.
Mechanism of drug action, Relationship between drug conc & effect, Receptors, Structural & families of receptors, Quantitation of drug receptor interaction & elicited effects
Unit 2 General Pharmacology (As per PCI syllabus)Mirza Anwar Baig
This document provides an overview of drug pharmacology and mechanisms of action. It discusses:
1) Drugs act by interacting with receptors on cells and initiating signal transduction pathways. This allows small drug signals to be amplified within cells.
2) There are four main families of receptors: ligand-gated ion channels, G protein-coupled receptors, enzyme-linked receptors, and intracellular receptors.
3) Drug effects depend on their intrinsic activity as full agonists, partial agonists, inverse agonists or antagonists. Antagonists can be competitive, irreversible or allosteric.
This document discusses different types of receptors including ligand gated ion channels, G-protein coupled receptors, enzyme linked receptors, and nuclear receptors. It describes receptor-drug interactions including affinity, intrinsic activity, efficacy, and potency. It defines different types of agonism and antagonism. The document provides examples and details on various receptor types and their mechanisms of action. In conclusion, extensive receptor pharmacology research has led to new drug targets, but more remains to be discovered about new receptor types and orphan receptors to further advance treatment options.
cell signaling is part of any communication process that governs basic activities of cells and coordinates multiple-cell actions. The ability of cells to perceive and correctly respond to their microenvironment is the basis of development, tissue repair, and immunity, as well as normal tissue homeostasis
This document discusses pharmacodynamics and the mechanisms of drug action. It explains that pharmacodynamics is the study of how drugs act on the body and their effects, focusing on drug-receptor interactions and the biochemical and physiological impacts of drugs. Various mechanisms are described, including stimulation, depression, irritation, and replacement effects. The key mechanisms of drug action are interactions with receptors, ion channels, enzymes, and transporter proteins. Different types of receptors - ligand-gated ion channels, G-protein coupled receptors, kinase-linked receptors, and nuclear receptors - are also outlined.
Shubham Sharma presented on the principles of pharmacodynamics at G.H.G Khalsa College of Pharmacy. Pharmacodynamics is the study of how drugs act on the body, including their biochemical and physiological effects. Drugs can act at the molecular, cellular, tissue and system levels. The main types of molecular drug targets include receptors, enzymes, ion channels, and nucleic acids. Drugs typically work by either directly binding to receptors or altering the activity of enzymes and ion channels. The main classes of receptors that drugs can target are ligand-gated ion channels, G-protein coupled receptors, enzyme-linked receptors, and nuclear receptors.
Advanced Medicinal Chemistry of GPCR Receptorsaurabh gupta
Contents:-
Introduction
Structure of G-protein
Signal Molecules / Ligands of GPCRs
G- Protein Mediated Pathways
Receptor Site Theories
Forces involved in drug receptor interactions
The document discusses the molecular mechanisms of action of drugs. It describes four main ways drugs produce effects in the body: 1) by acting on receptors, 2) by inhibiting carriers, 3) by modulating or blocking ion channels, and 4) by inhibiting enzymes. It focuses on describing the different types of protein targets for drug action, including receptors, ion channels, enzymes, and carrier molecules. It provides details on the structure and function of receptors, the main types of receptor families, and concepts such as receptor heterogeneity, subtypes, and the actions of agonists and antagonists.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
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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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
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- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
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2. CONTENTS IN BRIEF
1) Types of receptors
2) Cytoplasmic secondary messengers
3) Regulation of receptors
4) Drug receptor interaction
5) Diseases resulting from receptor malfunctioning
6) Significance of receptor subtypes
3. BRIEF INTRODUCTION
The relatively small number of biochemical mechanisms and
structural formats used for cellular signaling is fundamental to the
ways in which target cells integrate signals from multiple receptors
to produce additive, sequential, synergistic, or mutually inhibitory
responses.
The regulatory actions of a receptor may be exerted directly on its
cellular target(s), effector protein(s), or may be conveyed by
intermediary cellular signaling molecules called transducers.
4. TYPES OF RECEPTORS
1)Receptors as Enzymes: Receptor Protein Kinases and
Guanylyl Cyclases:
exert their regulatory effects by phosphorylating diverse effector proteins at the
inner face of the plasma membrane.
Most receptors that are protein kinases phosphorylate tyrosine residues in their
substrates. Eg: Insulin
are composed of an agonist-binding domain on the extracellular surface of the
plasma membrane, a single membrane-spanning element, and a protein kinase
domain on the inner membrane face.
For the receptors that bind atrial natriuretic peptides and the peptides guanylin and
uroguanylin, the intracellular domain is a guanylyl cyclase that synthesizes the
second messenger cyclic guanosine monophosphate (cyclic GMP), which activates
a cyclic GMP–dependent protein kinase (PKG) and can modulate the activities of
several cyclic nucleotide phosphodiesterases, among other effectors. Eg: ANP,
BNP
6. TYPES OF RECEPTORS:
2)Protease Activated Recptor signaling: Proteases that are
anchored to the plasma membrane or that are soluble in the extracellular
fluid(e.g. thrombin) can cleave ligands or receptors at the surface of cells to
either initiate or terminate signal transduction.
Eg: ACE inhibitors used for treatment of hypertension
3) Ligand gated ion Channels: These are most important
Receptors for several neurotransmitters form agonist-regulated ion-
selective channels in the plasma membrane, termed ligand-gated ion
channels or receptor operated channels, that convey their signals by
altering the cell’s membrane potential or ionic composition.
Eg: Acetyl Choline, Serotonin, GABA etc.
8. TYPES OF RECEPTORS:
4) G Protein Coupled Receptors:
G proteins are signal transducers that convey information (i.e., agonist
binding) from the receptor to one or more effector proteins. GPCRs include
diverse group of biogenic amines, eicosanoids and other lipidsignaling
molecules, peptide hormones, opioids, amino acids such as GABA, and
many other peptide and protein ligands.
Because of their number and physiological importance, GPCRs are the
targets for many drugs; perhaps half of all nonantibiotic prescription drugs
are directed toward these receptors that make up the third largest family of
genes in humans.
Central to the effect of many GPCRs is release of Ca2+ from intracellular
stores.
10. TYPES OF RECEPTORS:
5) Transcription Factors:
Receptors for steroid hormones, thyroid hormone, vitamin D, and the
retinoids are soluble DNAbinding proteins that regulate the transcription of
specific genes.
Regulatory sites in DNA where agonists bind are receptor-specific: the
sequence of a “glucocorticoid-response element,” with only slight variation, is
associated with each glucocorticoid-response gene, whereas a “thyroid-
response element” confers specificity of the actions of the thyroid hormone
nuclear receptor.
11. TYPES OF RECPTORS:
6) Cytoplasmic second messengers:
Binding of an agonist to a receptor provides the first message in
receptor signal transduction to effector to affect cell physiology. The
first messenger promotes the cellular production or mobilization of a
second messenger, which initiates cellular signaling through a
specific biochemical pathway.
Eg: cyclic AMP, cyclic GMP, cyclic ADP–ribose, Ca2+, inositol
phosphates, diacylglycerol, and nitric oxide (NO).
12. REGULATION OF RECEPTORS
Receptors not only initiate regulate biochemical events and physiological
function but also are themselves subject to many regulatory and
homeostatic controls.
These controls include regulation of the synthesis and degradation of the
receptor by multiple mechanisms, covalent modification, association with
other regulatory proteins, and/or relocalization within the cell. Transducer
and effector proteins are regulated similarly.
Modulating inputs may come from other receptors, directly or indirectly, and
receptors are almost always subject to feedback regulation by their own
signaling outputs.
13. REGULATION OF RECEPTORS
Continued stimulation of cells with agonists generally results in a state of
desensitization (also referred to as adaptation, refractoriness, or down-
regulation) such that the effect that follows continued or subsequent
exposure to the same concentration of drug is diminished.
This is also called as tachyphylaxis
Eg: Attenuated response to the beta receptor agonist in treatment of
asthma
Predictably, supersensitivity to agonists also frequently follows chronic
reduction of receptor stimulation.
Eg: following withdrawal from prolonged receptor blockade (e.g., the long-
term administration of b receptor antagonists such as propranolol )
14. DRUG RECEPTOR INTERACTION: TERMINOLOGY
Agonist : An agent which activates a receptor to produce an effect
similar to that of the physiological signal molecule.
lnverse agonist: An agent which activates a receptor to produce an
effect in the opposite direction to that of the agonist.
Antagonist: An agent which prevents the action of an agonist on a
receptor or the subsequent response,but doesnot have any effect of its
own.
Partial agonist: An agent which activates a receptor to produce
submaximal effect but antagonizes the action of a full agonist.
Ligand (Latin: ligare-to bind): Any molecule which attaches selectively
to particular receptors or sites. The term only indicates affinity or binding
without regard to functional change: agonists and
competitive antagonists are both ligands of the samereceptor.
15. RECEPTOR OCCUPATION THEORY:
Clark propounded a theory of drug action based on occupation of receptors
by specific drugs and that the pace of a cellular function can be altered by
interaction of these receptors with drugs which, in fact, are small molecular
ligands.
He perceived the interaction between the two molecular species,viz.drug
(D ) and receptor (R) to be governed by the law of mass action, and the
effect (E)to be a direct function of the drug-receptor complex (DR) formed:
D + R DR S E
16. Subsequently,it has been realized that occupation of the receptor is essential
but not itself sufficient to elicit a response. The agonist must also be able to
activate (induce a conformational change in) the receptor.
The ability to bind with the receptor designated as Affinity, and the capacity to
induce a functional change in the receptor designated as
intrinsic activity (IA) or efficacy are independent properties.
Competitive antagonists occupy the receptor but do not activate it. Moreover,
certain drugs are partial agonists which occupy and
submaximally activate the receptor.
An all or none action is not a must at the receptor. A theoretical
quantity(S) denoting strength of stimulus imparted to the cell was interposed
in the Clark‘s equation
17. Depending on the agonist, DR could generate a stronger or weaker S,
probably as a function of the conformational change brought about by the
agonist in the receptor.
Accordingly: Agonists have both affinity and maximal intrinsic activity (IA
= 1), e.g. adrenaline, histamine, morphine.
Competitive antagonists have affinity but no intrinsic activity (IA = 0),
e.g.propranolol, atropine, chlorpheniramine, naloxone.
Partial agonists have affinity and submaximal
intrinsic activity (IA between 0 and 1), e.g. dichloroisoproterenol (on
Badrenergic receptor), pentazocine (on p opioid receptor).
lnverse agonists have affinity but intrinsic activity with a minus sign
(IAbetween0 and-1), e.g.DMCM (on benzodiazepine receptor)
18. DISEASES RESULTING FROM RECEPTOR MALFUNCTIONING
Alteration in receptors and their immediate signaling effectors can be the
cause of disease.
The loss of a receptor in a highly specialized signaling system may cause a
relatively limited, if dramatic, phenotypic disorder (e.g., deficiency of the
androgen receptor and androgen insensitivity syndrome)
Deficiencies in widely employed signaling pathways have broad effects, Eg:
as seen in myasthenia gravis and some forms of insulin-resistant diabetes
mellitus, which result from autoimmune depletion of nicotinic cholinergic
receptors or insulin receptors, respectively.
19. SIGNIFICANCE OF RECEPTOR SUBTYPES
Molecular cloning has accelerated discovery of novel receptor subtypes,
and their expression as recombinant proteins has facilitated discovery of
subtype-selective drugs.
When selective ligands are not known, the receptors are more commonly
referred to as isoforms rather than as subtypes. The distinction between
classes and subtypes of receptors, however, often is arbitrary or
historical.
The a1, a2, and b receptors differ from each other both in ligand
selectivity among drugs and in coupling to G proteins (Gq, Gi, and Gs,
respectively), yet a and b are considered receptor classes and a1 and a2
are considered subtypes. The a1A, a1B, and a1C receptor isoforms differ
little in their biochemical properties, although their tissue distributions are
distinct.
20. Pharmacological differences among receptor subtypes are exploited
therapeutically through the development and use of receptor-selective
drugs.
Such drugs may be used to elicit different responses from a single
tissue when receptor subtypes initiate different intracellular signals, or
they may serve to differentially modulate different cells or tissues that
express one or another receptor subtype.
Increasing the selectivity of a drug among tissues or among responses
elicited from a single tissue may determine whether the drug’s
therapeutic benefits outweigh its unwanted effects.
21. THANK YOU
References:
Goodman and Gilman’s The Pharmacological basis
of Therapeutics 11th edition
K.D. Tripathy Essentials of medical Pharmacology
6th edition