Adrenergic agonists Sympathomimetic drugs. ANS Pharmacology Lecture 4 Dr. Hiwa K. Saaed College of Pharmacy/University of Sulaimani
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1 Adrenergic agonists Sympathomimetic drugs ANS Pharmacology Lecture 4 Dr. Hiwa K. Saaed College of Pharmacy/University of Sulaimani
2 Adrenergic agonists The adrenergic drugs affect receptors that are stimulated by norepinephrine or epinephrine. Adrenergic drugs act on adrenergic receptors, located either presynaptically on the neuron or postsynaptically on the effector organ NEP & EP are modulate the Rate and force of contraction of heart. Resistance (constriction and dilation) of blood vessels and bronchioles. Release of insulin, breakdown of fat (lipolysis). Therefore, they are frontline therapies for hypertension, depression, shock, asthma, angina & etc. 17 April
3 Neurotransmission at adrenergic neurons synthesis, storage, release, binding, removal (reuptake) of the neurotransmitter 1. Synthesis of norepinephrine: Tyrosine is transported by a carrier into the adrenergic neuron, Tyrosine hydroxylated by tyrosine hydroxylase to dihydroxyphenylalanine (DOPA). This is the rate-limiting step in the formation of norepinephrine. DOPA is then decarboxylated by the enzyme aromatic I-amino acid decarboxylase to form dopamine in the presynaptic neuron. 17 April
4 Neurotransmission at adrenergic neurons & drugs target: Synthesis and Storage of norepinephrine in vesicles: Dopamine is then transported into synaptic vesicles by an amine transporter system. This carrier system is blocked by reserpine. Dopamine is next hydroxylated to form norepinephrine by the enzyme dopamine β-hydroxylase. Release of norepinephrine: An action potential arriving at the nerve junction triggers an influx of calcium ions from the extracellular fluid into the cytoplasm of the neuron. The increase in calcium causes synaptic vesicles to fuse with the cell membrane and to undergo exocytosis to expel their contents into the synapse. Drugs such as guanethidine block this release. Binding to receptors: Norepinephrine binds to postsynaptic receptors or to presynaptic receptors. Adrenergic receptors use both the camp second messenger system and the phosphatidylinositol cycle to transduce the signal into an effect.
5 Neurotransmission at adrenergic neurons & drugs target: Removal of norepinephrine: 1. diffuse out of the synaptic space and enter the systemic circulation; 2. be metabolized to inactive metabolites by catechol-o-methyltransferase (COMT) in the synaptic space; or 3. undergo reuptake back into the neuron. Reuptake of norepinephrine into the presynaptic neuron is the primary mechanism for termination of its effects. The reuptake by the neuronal membrane involves a sodium-chloride (Na + /Cl - )-dependent norepinephrine transporter (NET) that can be inhibited by tricyclic antidepressants (TCAs), such as imipramine, by serotonin norepinephrine reuptake inhibitors such as duloxetine, or by cocaine. Potential fates of recaptured norepinephrine: it may be taken up into synaptic vesicles via the amine transporter system and be sequestered for release by another action potential, or it may persist in a protected pool in the cytoplasm. Alternatively, norepinephrine can be oxidized by monoamine oxidase (MAO) present in neuronal mitochondria.
6 Neurotransmission at adrenergic neurons & drugs target: Tyrosine hydroxylase can be inhibited by methyl-p-tyrosine. MAO: inhibitors of MAO (e.g., phenelzine, tranylcypromine) The mobile pool; many indirect-acting sympathomimetics (e.g., amphetamine, ephedrine, tyramine) can displace NE from the mobile pool Uptake: some indirect-acting sympathomimetics (cocaine, TCA). Presynaptic α 2 -receptors: (e.g., clonidine, alpha methyldopa) cause inhibition of NE release. Granular uptake of NE: blocker of granular uptake of NE (e.g., reserpine). NE release from granules: blockers (e.g., guanethidine). Postsynaptic receptors: can be activated or blocked. 17 April
7 Divided into subgroups on the basis of their Spectrum of action: α, β, or dopamine receptor affinity Mode of action: Direct, Indirect or both (Mix) Direct acting: I. α agonists: Non selective, α 1 -selective, α 2 -selective II. β agonists: Non selective, β 1 -selective, Β 2 -selective Indirect acting CAO in the synapse: Releaser: Amphetamine, tyramine Potentiate by MAOI, COMT blocker. Why? Reuptake inhibitor: Cocaine, TCA Mixed acting Ephedrine, metaraminol
8 Adrenoceptors Selective for NE & EP. dopamine can also activate some adrenoceptors at very high supraphysiologic concentrations. Divided into two main classes: α & β adrenoceptors All are members of GPCR superfamily. 17 April
9 α-receptors: EP NE>>Isoproterenol β-receptors: Isop>EP>NE 17 April
10 α-adrenoceptors (α 1 & α 2 ) α-receptors are subdivided into two subgroups α 1 & α 2, e.g., α 1 receptors have a higher affinity for phenylephrine than do α 2 receptors. Conversely, clonidine selectively binds to α 2 receptors and has less effect on α 1 receptors. α 1 Are present on the postsynaptic membrane α 2 Located primarily on presynaptic nerve endings. The stimulation of α 2 receptors causes feedback inhibition of the ongoing release of NE; α 2 Located on other cells such as the β-cell of the pancreas control insulin output. 17 April
11 β-receptors: Subdivided to β 1, β 2 and β 3 -receptors β 1 -receptors have ~equal affinities for both EP & NE., β 2 -receptors have higher affinity for EP than for NE. thus tissue with a predominance of β 2 -receptors (vasculature of skeletal muscle) are particularly responsive to hormonal effects of circulating EP released by adrenal medulla. Mechanism of action: binding of neurotransmitter at the β1 or β2-receptor result in activation of AC camp concentrations within the cell. 17 April
12 Mechanisms of action of adrenergic receptors : 17 April
13 Mechanisms of action of adrenergic receptors : 17 April
14 Desensitization of receptors: Prolonged exposure to the CAO reduces the responsiveness of the receptors due to: 1. Sequestration of the receptors 2. Down-regulation (destruction, or decreased synthesis) 3. An inability to couple to G-protein 17 April
15 Properties of Catecholamines& Noncatecholamines Catecholamines High potency in activating α & β receptors Rapid inactivation by: 1. COMT postsynaptically, gut wall, 2. MAO intraneuronally, liver or gut Thus, CAO have only a brief duration of action when given parenterally, and are ineffective when administered orally because of inactivation. Poor penetration into the CNS (polar) Noncatecholamines phenylephrine, ephedrine, amphetamine Have longer t 1/2 because they are not inactivated by COMT, and they are poor substrate for MAO Increased lipid solubility permits the greater access to the CNS
16 Major effects mediated by adrenoceptors Stimulation of α1 receptors characteristically produces vasoconstriction (particularly in skin and abdominal viscera) and an increase in total peripheral resistance and blood pressure. Stimulation of β1 receptors characteristically causes cardiac stimulation (increase in heart rate and contractility), whereas stimulation of β2 receptors produces vasodilation (in skeletal muscle vascular beds) and smooth muscle relaxation. 17 April
17 SITE OF ACTION 17 April
18 SITE OF ACTION 17 April
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