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Substance-Induced Vasodilatation in Vascular Smooth Muscles - Essay Example

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This essay "Substance-Induced Vasodilatation in Vascular Smooth Muscles" focuses on vascular smooth muscles that made up most of the blood vessels are lined by vascular endothelia. The vascular endothelium is a single layer of squamous cells that come in direct contact with blood. …
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Substance-Induced Vasodilatation in Vascular Smooth Muscles
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Substance-Induced Vasodilatation in Vascular Smooth Muscles Vascular smooth muscles, or muscles which made up most of the blood vessels, are lined by vascular endothelia. The vascular endothelium is a single layer of squamous cells which come in direct contact with blood. Aside from the function of serving as containment of blood, the endothelium secretes and produces vasoactive substances that cause blood vessels either to contract (vasoconstriction) or dilate (vasodilation or vasodilatation). These substances include: the prostacyclin, a muscle relaxant and inhibitor of platelet aggregation; the endothelin, a vasoconstrictor, and; EDRF or the endothelium-derived relaxing factor. The EDRF enables the relaxation of blood vessels eventually affiliated with the substance nitric oxide (NO) although there are other factors that can bring about vasodilatation like prostacyclin and endothelium-derived hyperpolarizing factor (Woods, Froelicher & Motze 2004; Bronzino 2000). EDRF is released by the vascular endothelium either spontaneously (basal release) or as a result of the stimulation of the endothelium by intracellular and extracellular factors. Release of EDRF by stimulation of the vascular endothelium may be induced by the following: blood flow; agonists; calcium; magnesium; calcium and inositol phosphates; mitochondrial ATP; cyclic GMP, and; protein kinase C (Ryan & Rubandi 1991 139). Many of the vasodilators in the market follow one principle or the other of endothelium stimulation to dilate the blood vessels and provide relief to elevated blood pressure. I Directly acting vasodilators are so called because they do not stimulate or act upon the nervous system to induce vasodilatation but directly act on the vascular smooth muscles. The advantage of direct acting vasodilators is that they diminish peripheral resistance and as a result normalize aberration in blood circulation which caused the elevation of the blood pressure. They also lower blood pressure whatever may be its causes because of their direct acting capability on the vascular smooth muscle. Unlike other antihypertensive agents, directly acting vasodilators do not result in side effects like hypotension and impotence. Their disadvantage however is that they cannot be used indefinitely and chronically because of the natural neuroendocrinic and autonomic reflexes of the human body that can compromise the fall in blood pressure (Craig & Stitzel 2003). . There is however no single or unified mechanism of action of vasodilators because different vasodilators act at different places and phases in the vascular smooth muscles. The calcium channel antagonists, for example, block the entry of calcium to the membranes of the vascular smooth muscle to prevent a calcium interaction with proteins in the muscle. Drugs like diazoxide and minoxidil activate potassium channels resulting in the hyperpolarization of cell membranes and ultimately blood vessel dilation. On the other hand, nitrovasodilator group of drugs, like nitroprusside, simulates the action of the tonic or basal method of EDRF release by the vascular endothelium, mainly the activation of the guanylate cyclase to increase the levels cyclic guanosine monophospahate (cGMP) in the cells (Craig & Stitzel 2003). Calcium-channel antagonists. Calcium channel antagonists which are direct acting vasodilating agents include such drugs as amlodipine, felodipine, nicardipine, nifedipine, nimodipine and nisoldipine. The common factor of this group is that they all act on the vascular smooth muscle to inhibit different calcium ionophores in the cell and intracellular membranes. They all primarily act to relax and dilate blood vessels and coronary muscles (Pinnock et al 2003). Potassium Channel Activators. Belonging to this group is the drug nicorandil. Potassium-channel activators induce directly acting effects on vascular smooth muscles by stimulating the opening of potassium channels within the cells of the blood vessels. The result is a hyperpolarization of the cell membranes and diminished electrical activity. These activities cause the blood vessels to dilate. Nicorandil specifically dilates arteries and lessens the resistance of these vessels (Pinnock et al 2003). Hydralazine. Hydralazine is a vasodilator that is dependent on the presence of an intact endothelium of a blood vessel. As such, it induces the release of nitric oxide (NO), the primary EDRF. It can also activate K channels which likewise help in vasodilatation (Craig & Stitzel 2003 p 228). Hydralazine primarily affects the smooth muscles of arteries rather than those of the veins, and is also believed to prevent the accumulation of intracellular free calcium, and promote potassium activity (Longnecker et al 2008). Minoxidil. Minoxidil is another directly acting vasodilator that works best on vascular smooth muscles of arteries. Together with diazoxide, minoxidil is referred to as potassium channel opener. This drug primarily acts on ATP-sensitive potassium channels in the plasma membrane of the vascular smooth muscle. The influx of potassium causes a hyperpolarization of the cell membrane which results in the relaxation of the blood vessels (Block & Beale 2004). Organic Nitrates and Nitrites. This group includes the likes of glyceryl trinitrate, isosorbide di- and mono-nitrate, nitric oxide, nitroprusside. As the nitrites and nitrates reach the vascular smooth muscles from the vascular lumen, the nitrates and sodium nitroprusside are converted to nitrites through a chemical reaction with some substances in the tissue. They then react with hydrogen ions and NO is produced. Another chemical reaction with thiols in the muscles produces nitrosothiols which incites guanylate cyclase to form guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGTP). The substance cGTP, as earlier discussed, directly causes the relaxation of the blood vessels (Pinnock et al 2003). Nitroprusside, one of the drugs belonging to this group, is one of the most effective blood-pressure lowering drugs. It differs from other directly acting vasodilators in that it acts on both vascular smooth muscles of arteries and veins. However, it is more often used in emergencies relating to elevated blood pressure because the drug is effective only for short durations. The mechanism of action of sodium nitroprusside is that it stimulates the production of nitric oxide or NO in situ, therefore raising the level of the cGMP which causes vasodilation (Block & Beale 2004). Diazoxide. Diazoxide is administered intravenously through injection and used, like sodium nitroprusside for the emergency treatment of elevated blood pressure because of its rapid acting nature (Block & Beale 2004). II A potential area worth looking into involving vascular myocytes relative to the treatment of cardiovascular disease would be the effect of magnesium into the vascular smooth muscles. This could prove relevant to the treatment of cardiovascular diseases considering that magnesium is a known calcium blocker. A study done in 2001 showed that magnesium dilates “both the epicardial and resistance coronary arteries” and although the vasodilatation effect of magnesium is independent of epithelium-derived-nitric oxide, there is a possibility that it has something to do with another vasodilation substance called prostacyclin. In this study, the researchers have proven the potential valuable contribution of magnesium in the treatment of cardiovascular diseases (Teragawa et al 2001). References Block, J & Beale, J 2004, Wilson and Gisvold’s Textbook of Organic Medicinal and Pharmaceutical Chemistry, Lippincott Williams & Wilkins, pp 653-654 Bronzino, J D. 2000, The biomedical engineering handbook, CRC Press, pp 31-38. Craig, CR, Stitzel, R 2003, Modern pharmacology with clinical applications, Lippincott Williams & Wilkins, p 223, 227-228. Longnecker, DE & Brown, DL & Newman, MF & Zapol, W 2008, Anesthesiology, McGraw-Hill Professional, p 192. Pinnock, C, Lin T, Smith T, Jones, R 2003, Fundamentals of Anaesthesia, Cambridge University Press, p 691-692. Ryan, U S, Rubanyi, GM 1991, Endothelial Regulation of Vascular Tone, Informa Health Care, Teragawa,H & Kato, M & Yamagata, T & Matsuura, H & Kajiyama, G 2001, Magnesium causes nitric oxide independent coronary artery vasodilation in humans, http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1729866&blobtype=pdf Woods, S , Sivarajan, E, Froelicher E, & Motzer, SA 2004, Cardiac Nursing, Lippincott Williams & Wilkins, p 54. Read More
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