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Free serotonin (5-hydroxytryptamine; 5-HT) levels in blood are kept low because platelets avidly trap the autacoid released from neuronal or enterochromaffin cells. If platelets aggregate and release serotonin at sites of atheroma or endothelium denudation, the artery wall will generally constrict. The discovery that endothelial cells can release endotheliumderived relaxing factor (EDRF), a powerful relaxant now known to be NO (Palmer et al., 1987), has stimulated much work in trying to unravel the complex interactions that can occur for serotonin within the artery wall in large and small vessels.

This brief review describes studies in our laboratory aimed at determining what changes may occur to the reactivity to serotonin in the coronary artery (a) when there is an acute loss of endothelium, and (b) if the arteries are in an atheromatous or atherosclerotic-like state. In addition, the effect of hypertension and medial hypertrophy on the reactivity of serotonin in the rabbit hindquarter was tested. Here, paradoxically, serotonin is a vasodilator of this intact vascular bed, presumably at the level of the small resistance vessels.