Abstract
Abstract Serotonin is a potent direct constrictor of most vascular smooth muscle (mainly by activating 5HT2A-serotonergic receptors), but also acts a strong agonist at endothelial cells. Aggregating platelets release serotonin in amounts sufficient to activate both cell types. When platelet-derived serotonin reaches healthy endothelial cells, it binds to 5HT1D-cell membrane receptors, coupled by Gi-proteins to activation of endothelial nitric oxide synthase. The resulting release of nitric oxide not only limits aggregation but prevents contractions of the vascular smooth muscle cells; at the chronic level, serotonin contributes to the atheroprotective role of the endothelium. When the endothelium regenerates in vivo, it becomes dysfunctional and selectively loses the Gi-protein-mediated response to serotonin, whether exogenous or released from aggregating platelets; as a consequence, acute vasospasm is facilitated and local atherosclerosis ensues. Whereas these responses are well established in systemic (in particular coronary) arteries, their relevance in the cerebral circulation remains to be established.
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