Cardiovascular effects of serotonin.

The major target for circulating serotonin (released from aggregating platelets) appears to be the blood vessel wall (although little evidence is available), suggesting a role for the monoamine in controlling cardiac function. In cerebral blood vessels, serotonergic neurons are present, implying a potential serotonergic neurogenic control. Serotonin causes contraction of most large arteries and veins; it also causes contraction of venules. This is due mainly to direct activation of vascular smooth muscle, although amplification of the response to other endogenous vasoconstrictors (e.g., angiotensin II and norepinephrine) as well as facilitated release of norepinephrine may contribute. In peripheral blood vessels, the receptors mediating the contractions evoked by serotonin belong mainly to the 5-HT2-serotonergic subtype; in the coronary and cerebral arteries, this need not be the case. Vasodilator responses to serotonin are seen mainly at the arteriolar level, but they can also be observed in larger blood vessels. They can be caused by the release of other endogenous vasodilators (e.g., vasoactive intestinal polypeptide), direct relaxation of vascular smooth muscle, inhibition of adrenergic neurotransmission, or production of endothelium-derived relaxing factor(s). The dilator responses to serotonin are mediated by receptors with characteristics similar to 5-HT1-serotonergic binding sites. Aggregating platelets release enough serotonin to evoke both constrictor and dilator responses. The absence of endothelium may change the primary response to aggregating platelets from relaxation to contraction. The responsiveness of the blood vessel wall to serotonin can be augmented acutely by local hypoxia or by cooling. It is exaggerated in blood vessels taken from hypertensive or atherosclerotic animals.(ABSTRACT TRUNCATED AT 250 WORDS)