Serotonin functions as a neurotransmitter, is synthesized in the gastrointestinal mucosa, and is stored primarily in platelets and the endothelium of the lungs and central nervous system. It’s role in the central regulation of blood pressure is mediated by receptors and is subsequently dependent on their availability. In large arteries, serotonin combined with S2 binding sites produces vasoconstriction. Agents that block this process catalyze a vasodilatory response in the vessel counteracting the vasoconstricting impact of serotonin.
In cases where atherosclerosis is present endothelium may be dysfunctional or absent, allowing exogenous serotonin or serotonin released as a result of platelet aggregation to induce vasoconstriction, coronary spasm, or vasospasm in the saphenous vein grafts. In combination with catecholamines or angiotensin II this effect may be synergistic and much more profound.
Serotonin antagonists such as Ketanserin provide an anti-hypertensive effect without reflex tachycardia often associated with agents such as sodium nitropresside, nitroglycerin, or hydralazine. It has been utilized to reduce perioperative hypertension associated with cardiac surgery by reducing systemic and pulmonary vascular resistance while promoting a mild increase in cardiac output. Ketanserin prevents serotonin induced vasoconstriction in atherosclerotic arteries, and exhibits a vasodilatory effect in normal coronary vessels.
Van der Starre PJ, Renneman RS. The role of serotonin blockers in cardiac anesthesia. Journal of Cardiothoracic and Vascular Anesthesia. 1994;8:455-462.
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