The present study was undertaken to assess in unanesthetized rats the effect of a kinin antagonist (D-Arg-Arg-Pro-Hyp-Gly-Thi-Ser-D-Phe-Thi-Arg-trifluoroacetic acid) on blood pressure, heart rate, and splanchnic nerve activity. The antagonist infused intra-arterially (50 micrograms/min) for 10 min had no blood pressure effect in control rats. It did, however, cause a significant increase in blood pressure in animals preinfused with a nonpressor dose of angiotensin II (1 ng/min i.v.) for 70 min. The antagonist-induced blood pressure rise was not associated with an increase in splanchnic nerve activity. Acute angiotensin-converting enzyme (ACE) inhibition with captopril (2.5 mg i.v.) had no influence on the pressor response to the kinin antagonist in angiotensin II-treated rats. These results obtained in conscious normotensive rats suggest that endogenous kinins participate in the control of blood pressure by attenuating the vasoconstrictor effect of angiotensin II. The involvement of kinin does not seem to be enhanced by acute ACE inhibition.