Serotonin and arterial vessels.
The vasoconstrictor effects of serotonin can be explained by (a) activation of serotonergic receptors on vascular smooth muscle, (b) activation, directly or indirectly, of postjunctional alpha-adrenoceptors, and (c) amplification of the response to other vasoactive agonists. Vasoconstrictor responses to serotonin may play a role in the etiology of vasospasm and in the maintenance of the augmented peripheral resistance in arterial hypertension. The vasodilator effects of serotonin can be caused by (a) inhibiting vascular smooth muscle directly, (b) releasing other inhibitory substances, such as vasoactive intestinal polypeptide, (c) inhibiting adrenergic neurotransmission, and (d) triggering of endothelium-dependent relaxation.
D000818:Animals; D001158:Arteries / Q000502:physiology*; D003331:Coronary Vessels / Q000502:physiology; D004727:Endothelium / Q000166:cytology; D006801:Humans; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D012701:Serotonin / Q000494:pharmacology / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
D012701:Serotonin