Vascular conductance in the mesenteric, hindquarter, and renal beds of the conscious rabbit was derived from regional blood flow (pulsed Doppler
flowmeter) and ear artery pressure. After autonomic ganglion blockade (
mecamylamine),
serotonin (5-HT, 5-hydroxytryptamine) infusion, 3-60 micrograms/kg/min i.v., dilated the mesenteric and hindquarter beds but caused renal blood flow to fall to zero. Angiography confirmed that
serotonin had caused the conduit renal arteries to
spasm. This response was unaltered by 1 mg/kg
prazosin but was antagonised by 0.5 mg/kg
ketanserin and 0.5 mg/kg
methysergide. Only the latter
drug shifted the dilator-response curves in the other two beds.
Methiothepin, 1 mg/kg, flattened both the dilator and constrictor response curves, perhaps by binding to an allosteric site on the
serotonin receptor.
5-Carboxamidotryptamine (5-CT) caused about half the renal arteries to
spasm at less than 30 ng/kg/min and dilated the other beds. From the antagonist data, we suggest that 5-HT2 receptors mediate the contraction of the renal artery, but that "5-HT1-like" receptors mediate the dilatation in the renal, mesenteric, and hindquarter beds in the conscious rabbit. 5-CT is not helpful in defining the receptors in the renal artery. The rather special spasmogenic response to
serotonin in the renal artery is worthy of further research to reveal what factors may lead to large artery
spasm.