PHC 313 The 7 th. Lecture. Adrenergic Agents
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1 PHC 313 The 7 th. Lecture Adrenergic Agents
2 Introduction
3 Introduction Adrenergic agents are a broad class of agents employed in the treatment of many disorders. They are those chemical agents that exert their pharmacological and therapeutic effects by acting at the peripheral sites of the sympathetic division of the autonomic nervous system. In general, stimulation of the sympathetic nervous system causes what is known as "fight-or-flight" responses.
4 Introduction Fight & flight responses include an increased rate and force of heart contraction, a rise in blood pressure, a shift of blood flow to muscles, dilation of bronchioles and pupils, and an increase in blood glucose levels through gluconeogenesis and glycogenolysis.
5 Norepinephrine Drugs can influence adrenergic responses through a variety of mechanisms, and an understanding of these mechanisms requires knowledge regarding the details of norepinephrine biosynthesis, storage, release, and fate following release. NE is the adrenergic neurotransmitter that is liberated from postganglionic sympathetic neurons as a result of sympathetic nerve stimulation..
6 NE & Epinephrine Epinephrine is also an endogenous adrenergic neurotransmitter but it is not released from sympathetic nerve endings as NE. Epinephrine is synthesized and stored in adrenal medulla from which it is released into circulation to various organs and tissues where it exerts its effects at adrenergic receptor sites; and is often known as neurohormone.
7 Chemistry Norepinephrine and epinephrine are members of a class of pharmacologically active substances known as catecholamines, because they contain within their structures both an amine and 3,4-dihydroxybenzene, which is known by the common chemical name of catechol.
8 Biosynthesis of NE Catecholamine biosynthesis takes place in the following places: adrenergic and dopaminergic neurons in the central nervous system sympathetic neurons in autonomic nervous system adrenal medulla. The biosynthetic steps, substrates and enzymes involved are shown in the following figure:
9 Biosynthesis of NE
10 Biosynthesis of NE Norepinephrine biosynthesis takes place by a three-step process: 1. Conversion of tyrosine to L-dihydroxyphenylalanine (L-DOPA) catalyzed by tyrosine hydroxylase. This step is the rate-limiting process in catecholamine biosynthesis. 2. Decarboxylation of L-DOPA to produce dopamine catalyzed by L-DOPA decarboxylase. 3. Stereospecific hydroxylation of dopamine to produce NE catalyzed by dopamine β-hydroxylase In the adrenal medulla, a 4 th biosynthetic reaction takes place by which NE is converted to epinephrine catalyzed by phenylethanolamine N-methyltransferase (PNMT).
11 Storage & Release Norepinephrine is stored in the vesicles, the norepinephrine remains in the vesicles until released into the synapse during signal transduction. When a wave of depolarization reaches the terminus of an adrenergic neuron, it triggers the transient opening of voltage-dependent calcium channels, causing an influx of Ca 2+ which triggers fusion of the storage vesicles with the neuronal cell membrane, spilling the norepinephrine and other contents of the vesicles into the synapse through exocytosis.
12 Fate of NE Once it has been released and is stimulating its various receptors, there must be mechanisms for removing the norepinephrine from the synapse and terminating the adrenergic impulse. The action of NE at adrenergic receptors is terminated by a combination of processes including: 1. Reuptake into neurons(uptake 1). 2. Diffusion away from the synapse (uptake-2). 3. Metabolism. Termination of epinephrine activity occurs mostly via metabolism.
13 Uptake Mechanisms NE is uptake into the presynaptic neuron. Up to 95% of released norepinephrine is removed from the synapse by this mechanism (uptake-1) Part of the norepinephrine taken into the presynaptic neuron by uptake-1 is metabolized and part of it is restored in the storage vesicles to be used again as neurotransmitter.
14 Uptake Mechanisms Uptake-2 mechanism operates in a variety of other cell types but only in the presence of high concentrations of norepinephrine. That portion of released norepinephrine that escapes uptake- 1 diffuses out of the synapse and is metabolized in extraneuronal sites.
15 Metabolism of NE Two principal enzymes involved in catecholamines metabolism are the monoamine oxidase (MAO) and catechol O-methyltransferase (COMT). MAO has role in the metabolism of intraneuronal catecholamines COMT acts primarily upon catecholamines that enter the circulation and the extraneuronal tissues.
16 Metabolism of NE MAO acts via oxidative deamination of catecholamines. R CH 2 NH 2 R CH NH R CHO + NH 4 Other nzymes involve in metabolism of Norepinephrine : MAO, monoamine oxidase COMT, catechol-o-methyltransferase AR, aldehyde reductase AD, aldehyde dehydrogenase.
17 Metabolism of NE
18 Metabolism of NE Norepinephrine is initially metabolized to DOPGAL (DOPGAL, 3,4-dihydroxyphenylglycolaldehyde) by monoamine oxidase and to normetanephrine by catechol-omethyltransferase. Each of the initial products may, in turn, be further metabolized and these metabolites are subject to further metabolism via phase II conjugation.
19 Adrenergic Receptors
20 Adrenergic Receptors Following its release, norepinephrine diffuses through the intercellular space to bind reversibly to adrenoceptors on the effector cell, inducing a conformational change in the receptor. This conformational change triggers a biochemical cascade that results in a physiologic response by the effector cell. Each adrenoceptor is coupled through a G-protein to an effector mechanism.
21 Adrenergic Receptors Adrenergic receptors were subclassified into α- and β- adrenoreceptor classes according to their responses to different adrenergic receptor agonists, principally norepinephrine, epinephrine, and isoproterenol.
22 Adrenergic Receptors These catecholamines are able to stimulate α-adrenoceptors in the following descending order of potency: epinephrine > norepinephrine > isoproterenol In contrast, β-adrenoceptors are stimulated in the following descending order of potency: isoproterenol > epinephrine > norepinephrine.
23 Adrenergic Receptors In addition to the receptors on effector cells are adrenoreceptors that respond to norepinephrine (α 2 -receptors) on the presynaptic neuron, which, when stimulated by norepinephrine, act to inhibit the release of additional norepinephrine into the synapse.
24 Summary of NE Cycle
25 Adrenergic Receptors The receptors activation may result in: 1. α 1 -Adrenergic Receptors: Vasoconstriction (so they B.P. ), relaxation of GIT smooth muscle, salivary secretion and hepatic glycogenolysis. Thus used in treatment of HYPOTENSION 2. α 2 -Adrenergic Receptors: Transmitter release, including Ach, NE from the autonomic nerves (i.e., it sympathetic responses) Thus, used in treatment of HYPERTENSION
26 Adrenergic Receptors 3. β 1 -Adrenergic Receptors: Cardiac rate and force and relaxation of GIT smooth muscle. Thus, used in treatment of heart failure and shock. 4. β 2 -Adrenergic Receptors: Bronchodilatation, vasodilatation and smooth muscle relaxation. Also uterine contraction, hepatic glycogenolysis and muscle tremors. Thus, used in treatment of asthma and during premature labour
27 Adrenergic Receptors Generally α 1 stimulation α 2 stimulation β 1 stimulation β 2 stimulation contraction of smooth muscle (Excitatory). relaxation of GIT smooth muscles (inhibitory). stimulation in heart (Excitatory). relaxation of smooth muscle (inhibitory).
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