Adrenergic receptors and drugs.pptx
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This document discusses adrenergic receptors and non-anesthetic drugs that act on them. It describes the types and locations of beta-1 and beta-2 receptors, and how beta blockers work by selectively binding to these receptors to decrease heart rate, contractility, and conduction times. It also discusses the pharmacokinetics of beta blockers, including their absorption, distribution, metabolism and excretion, which depends on lipid solubility. Finally, it outlines several types of second messengers involved in G protein-coupled receptor signaling, such as cAMP, cGMP, IP3, DAG and calcium ions.
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Dr. Jibachha Sah,M.V.Sc( Veterinary pharmacology, TU,Nepal),posted lecturer notes on AUTONOMIC AND SYSTEMIC PHARMACOLOGY for B.V.Sc & A.H. 6 th semester veterinary students of College of veterinary science,Nepal Polytechnique Institute, Bharatpur, Bhojard, Chitwan, Nepal.I hope this lecture notes may be beneficial for other Nepalese veterinary students. Please send your comment and suggestion .Email:jibachhashah@gmail.com,moble,00977-9845024121
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- 2. types of Adrenergic receptors
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- 4. Mechanism of Action ►Beta-1 receptors are primarily found in cardiac nodal tissue, cardiac myocytes, other heart conduction pathway tissues, and kidneys. ►Beta- receptors are G-protein-coupled receptors (specifically Gs alpha subunit) whose action is exerted through the cyclic AMP (cAMP) and cAMP-dependent protein kinase action with resultant calcium ion concentration increases. ►Increased intracellular calcium increase inotropy in the heart through calcium-induced exchange facilitated by the sarcoplasmic reticulum. ►Myosin light chains phosphorylated by PKA lead to contractility in muscle cells. ►Normally, activation of the beta-1 receptor in the heart increases sinoatrial (SA) nodal, atrioventricular (AV) nodal, increased heart rate and contractility. Stroke volume and cardiac output will also increase
- 5. blockers exert their effect by binding to the beta- receptor sites selectively and inhibiting the action of epinephrine and norepinephrine on these sites. ◦ decreased contractility (inotropy) ◦ decreased heart rate (chronotropy) ◦ increased relaxation (lusitropy) ◦ decreased cardiac conduction times (dromotropy).
- 6. Pharmacokinetics ABSORPTION/ DISTRIBUTION • Low lipid solubility, e.g. atenolol poorly absorbed from gut • Higher lipid solubility, e.g. metoprolol = well absorbed, but cross BBB and ↑ CNS side-effects METABOLISM AND EXCRETION • Low lipid solubility = minimal hepatic metabolism and excreted unchanged in urine • High lipid solubility = hepatic metabolism
- 7. Second messengers There are several types of second messengers, including: 1-cyclic adenosine monophosphate (cAMP) Gs & Gi 2- cyclic guanosine monophosphate (cGMP) 3- inositol triphosphate (IP3) 4-diacylglycerol (DAG) 5-calcium ions (Ca2+).
- 8. Second messengers • cAMP is activated by Gs proteins cAMP is produced from ATP by the enzyme adenylate cyclase. Inhibition of Gs receptors will also reduce the cAMP concentrations i.e. beta blockers • cAMP is inhibited by Gi proteins These may act as agonists through Gi coupled receptors to increase cAMP; as an example: α2 agonism with clonidine mu receptors with opioids.
- 9. Second messengers • IP3 and DAG are activated by Gq proteins Inositol triphosphate increase in cytoplasmic calcium concentration can trigger a variety of downstream signaling events, including muscle contraction (e.g. via stimulation of α1 adrenoceptors and muscarinic acetylcholine receptors). • cGMP is activated by nitric oxide. NO is a gas that is produced by the enzyme nitric oxide synthase (NOS). It diffuses across cell membranes and can activate the enzyme guanylate cyclase, which produces the second messenger cyclic GMP (cGMP). • Calcium ions (Ca2+): In addition to being released from the ER in response to IP3 They can modulate a variety of cellular processes, including muscle contraction, enzyme activity, and gene expression.