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Competitive Antagonism - Essay Example

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Acetylcholine (ACh) stimulates the contraction of skeletal muscle via nicotinic receptors and the contraction of smooth muscle via muscarinic receptors. Muscarinic receptors belong to the 7TM superfamily (seven transmembrane spanning superfamily) of G-protein linked receptors…
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Competitive Antagonism
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Competitive Antagonism Discuss how ACh produces a contraction in smooth muscle, details of mechanism and second messenger involved. Acetylcholine(ACh) stimulates the contraction of skeletal muscle via nicotinic receptors and the contraction of smooth muscle via muscarinic receptors. Muscarinic receptors belong to the 7TM superfamily (seven transmembrane spanning superfamily) of G-protein linked receptors and are of the M1- M5 subtypes, depending on the type of smooth muscle they are located in. The ACh dependant response of the muscarinic receptors is mediated through GTP binding proteins. In the M1, M3 and M5 subtypes, the Gq family of G-proteins is involved in the activation of PLC (phospholipase C). Here, ACh is the agonist of muscarinic receptors.
Mechanism of smooth muscle contraction – When ACh stimulates the G-protein coupled muscarinic receptors, a conformational change occurs, leading to the activation of the G-protein. The activated G-protein activates the intracellular enzyme, PLC (phospholipase C). This enzyme in turn hydrolyses PI(4,5)P2 (phosphatidylinositol-4,5-bisphosphate). This hydrolysis results in the production of two compounds – DAG (diacylglycerol) and IP3 (inositol-1,4,5-triphosphate). IP3 is soluble and diffuses through the cytosol. It binds to receptors on the endoplasmic reticulum resulting in the release of calcium ions (Ca2+) from the intracellular stores. The rise in intracellular calcium ions results in contraction of the smooth muscle. This happens when the intracellular calcium ions bind to calmodulin and activate it. Activation of calmodulin results in activation of the myosin light-chain kinase (MLCK) enzyme by the calcium-calmodulin complex, which then catalyzes the transfer of phosphate group from ATP to myosin cross bridges. The phosphorylated myosin cross bridges then interact with actin, causing shortening of the fiber. This results in muscle contraction. The cross-bridge cycle is powered by ATP.
Second messenger involved - IP3 (inositol-1,4,5-triphosphate) is the second messenger, as it relays the signal from outside the cell to the inside, resulting in the release of calcium ions that cause muscle contraction.
(Gomperts, Kramer & Tatham 2009; Marieb & Hoehn 2010)
2. Discuss how Ad produces relaxation of pre-contracted smooth muscle, details of mechanism and second messenger involved.
Acetylcholine (ACh) and adrenaline (Ad) are two agonists whose actions are independent of one another and result in opposite effects. Ad brings about the relaxation of pre-contracted smooth muscle by acting via the G-protein coupled β-adrenergic receptors on the cells.
Mechanism of Ad induced relaxation of pre-contracted smooth muscle – Ad binds to the G-protein linked β-adrenergic receptor causing a conformational change in the G-protein. This activates the enzyme adenylate cyclase. Adenylate cyclase converts ATP to cAMP (cyclic AMP). cAMP in turn activates the enzyme PKA (protein kinase A). PKA is regulated by the amount of cAMP in the cell and so, it is also called cAMP dependant protein kinase. The activated enzyme PKA phosphorylates myosin light-chain kinase (MLCK) in the muscle cells. When MLCK is phosphorylated, it has low affinity for calcium-calmodulin complex (Ca2+–calmodulin).
During muscle contraction, calcium-calmodulin complex activates MLCK, which then catalyzes the transfer of phosphate group from ATP to myosin cross bridges that then interact with actin resulting in muscle contraction. However, when MLCK is phosphorylated and has low affinity for the calcium-calmodulin complex, it can no longer cause the phosphorylation of myosin cross bridges. This results in the relaxation of pre-contracted smooth muscles.
Second messenger involved - cAMP is the second messenger involved in this mechanism as it relays the signal from the outside of the cell to the inside, resulting in activation of PKA that causes smooth muscle relaxation.
(Baker, Murray & Baker 2001; Marieb & Hoehn 2010)
References
Baker, R, Murray, R, and Baker E 2001, PDQ biochemistry, Volume 1, BC Decker Inc, Ontario.
Gomperts, B, Kramer, I, and Tatham, P 2009, Signal transduction, Academic Press, London.
Marieb, E & Hoehn, K 2010, Human anatomy and physiology, Pearson Education, New Jersey. Read More
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