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Abstract:
The complexity of the vascular effects of 5-hydroxytryptamine (5-HT) is illustrated by differences in sensitivity to the amine among arterial tissues of different origin. The interaction of 5-HT with 5-HT2 receptors is inhibited by specific antagonists such as ketanserin and methysergide. Such compounds also inhibit the contractile responses to endogenous 5-HT released from aggregating platelets. The vasodilator component of the response to 5-HT can be unmasked in the presence of serotonergic blockade, provided the antagonist used has no partial agonistic properties. 5-HT augments (amplifies) the vasoconstrictor responses to adrenergic and nonadrenergic neurohumoral mediators. The amplifying effect of the monoamine is prevented by 5-HT2-serotonergic antagonists such as ketanserin.