Renal vasoconstrictor response to 5-hydroxytryptamine in the in situ autoperfused rat kidney: involvement of angiotensin II and the 5-HT2 receptor activation.

Using a number of agonist and antagonist compounds, we attempted to characterize the responses and receptors involved in the effects of 5-hydroxytryptamine (5-HT) in the in situ autoperfused rat kidney. An intra-arterial (i.a.) bolus injection of 5-HT (0.0125 to 0.1 microg/kg) increased renal perfusion pressure in a dose-dependent way but did not change the systemic blood pressure. The 5-HT2 receptor agonist, (1-(3-chlorophenyl) piperazine), m-CPP, caused a local vasoconstrictor effect in the autoperfused rat kidney. An intra-arterial injection of 5-carboxamidotryptamine, 5-CT and 1-(m-chlorophenyl)-biguanide (m-CPBG) did not modify the renal perfusion pressure. The vasoconstrictor effect elicited by 5-HT and m-CPP was significantly decreased by ritanserin, enalapril and losartan but was not modified by prazosin, propranolol or indomethacin pretreatment. Our data suggest that the vasoconstrictor serotonergic response induced in the in situ autoperfused rat kidney is mediated through angiotensin II activation by a local 5-HT2 receptor mechanism.