Adrenoceptors and sympathomemtics - Essay Example

Adrenoceptors and Sympathomemtics Adrenoceptors and Sympathomemtics Adrenoceptors are the receptors, which epinephrine, norepinephrine and sympathomimetic drugs interact with in transmission of information. All adrenoceptors have G protein linking them to their effector system. Linking of the G protein is through reversible interaction with loop of receptor protein. The Classification of adrenergic receptors forms two groups, which include Alpha adrenoceptors and Beta adrenoceptors (Foye, Lemke, and Williams, 2008, p. 396). Classification of alpha adrenoceptors into α1 and α2 considers their location and functions.

Location of the alpha-1 receptors in the neural system is in postsynaptic nerve terminal while alpha-2 receptors are in presynaptic nerve terminal. In the vascular and smooth muscle cell, the alpha-2 adrenergic receptors are located in the postsynaptic terminal. Most of α 1-adrenoceptors activation are linked to excitation of postsynaptic target α-2-adrenoceptors usually activates the Gi inhibitory protein that in turn decreases cAMP. The inhibitory function of alpha-2 adrenergic receptors is vital negative feedback system to control of the discharge of presynaptic nerve terminal’s noradrenaline.

These prevent prolonged activation of the effector organs such as male sex organs, eyes and veins (Bryant, Knights and Salerno, 2010, p. 209). These alpha-adrenergic receptors usually control the vasoconstriction of arterioles in skin, pupil dilation, gut relaxation and smooth muscle relaxation in the prostrate and bladder neck. Classification of beta-adrenergic receptors into β1, β2 and β3 considers their affinity to agonist or antagonist. Location of site that recognises agonist and antagonist is in the portion of receptor that is membrane-bound.

Distribution of Beta-adrenergic receptors is in various tissues. Beeta-1 is in the heart, beta-2 in the smooth muscle and beta-3 in adipocytes cell membrane (Bryant, Knights and Salerno, 2010, p. 210). All of the beta-adrenergic receptors lead to activation of adenylyl cyclase in which the agonists leads to formation of cAMP from ATP. Activation these receptors leads to increase heart beat rate, relaxed bronchus and uterine and vasoconstriction of arterioles supplying blood to skeletal muscle.

Sympathomimetic drugs are those designed to act similarly like adrenaline or noradrenaline by their action on adrenoceptors and act in sympathetic stimulation of the system (Bertram and Anthony, 2009, p. 128). The classification of these drugs as direct or indirect agonist depends on their mode of action in stimulation of the neural sympathetic system. Direct agonist act by interacting with the adrenoreceptors and activating them to cause stimulation of nervous sympathetic system like dobutamine (Bryant, Knights and Salerno, 2010, p. 211). Indirect agonist drugs act through two ways.

In the first way, they can act by displacing catecholamine stored in the terminal nerve ending in to the cytoplasm like in the action of tyramine (Neal, 2012, p. 25). In the second way, the drugs may reduce reuptake of catecholamine released to the synaptic cleft in the nerve system an action seen in cocaine. Some may also act by reducing enzymatic degradation of the noradrenaline or adrenaline released to the synaptic cleft. In both ways in indirect sympathomimetic drugs lead to increased endogenous catecholamine in synaptic cleft (Oconnell, Blair, and Pedigo, 2014, p. 41).Through the action of direct agonist type of drug, stimulation of the sympathetic system takes place without requirement of endogenous catecholamine.

In the action of indirect agonist drugs, the action make sure the amounts of catecholamine in the synaptic cleft is increased and remain high to activate the sympathetic nervous system. Action of catecholamine or sympathetic drugs on alpha and beta-adrenergic receptors has an additive effect on the sympathetic system. ReferencesBertram K. & Anthony T. (2009). Basic and Clinical Pharmacology 11e. New York, McGraw Hill.Bryant, B. J., Knights, K. M., & Salerno, E. (2010). Pharmacology for health professionals.

Chatswood, N.S.W., Elsevier Australia.Foye, W. O., Lemke, T. L., & Williams, D. A. (2008). Foyes principles of medicinal chemistry. Philadelphia, Lippincott Williams & Wilkins.Neal, M. J. (2012). Medical pharmacology at a glance. Chichester, West Sussex, Wiley-Blackwell.Oconnell, T. X., Blair, T., & Pedigo, R. (2014). Crush step 1: the ultimate USMLE step 1 review. Philadelphia, PA : Elsevier Saunders