5-hydroxytryptamine and precapillary vessels.
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.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D015237:Dinoprost; D004347:Drug Interactions; D006632:Histamine / Q000494:pharmacology; D007650:Ketanserin; D008784:Methysergide / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D010880:Piperidines / Q000494:pharmacology; D011460:Prostaglandins F / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism; D012701:Serotonin / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects*
D010880:Piperidines; D011460:Prostaglandins F; D011942:Receptors, Adrenergic, alpha; D000804:Angiotensin II; D012701:Serotonin; D006632:Histamine; D007650:Ketanserin; D015237:Dinoprost; D009638:Norepinephrine; D008784:Methysergide