Bolus injections of bradykinin (BK, 0.25-1.0 nmol.kg-1 intraarterially (i.a.)) in anesthetized rats produced a dose-dependent hypotensive response, while desArg9-BK (0.25-1.0 nmol.kg-1 i.a.), Lys-desArg9-BK (0.25-1.0 nmol.kg-1 i.a.), and Sar[D-Phe8]desArg9-BK (0.5-1.0 nmol.kg-1 i.a.) were inactive. At 12-24 h after the pretreatment with lipopolysaccharide (10-100 micrograms.kg-1 i.v.), BK produced a greater decrease in blood pressure than in nontreated rats and Sar[D-Phe8]desArg9-BK (0.5-1.0 nmol.kg-1 i.a.) decreased blood pressure by 13.0 +/- 1.0 and 22.2 +/- 2.31 mmHg (1 mmHg = 133.3 Pa), whereas both desArg9-BK and desArg10-kallidin were inactive. The hypotensive effect of BK (0.25-1.0 nmol.kg-1 i.a.) was significantly reduced by HOE-140 (1.0 nmol.kg-1 i.a.) given 5 min before and that of Sar[D-Phe8]desArg9-BK was reduced by [Leu8]desArg9-BK (1.0 nmol.kg-1 i.a.) given 3 min before the agonists. These results indicate that in rats lipopolysaccharide induces B1 receptors in 18 to 24 h. B1 agonists protected from degradation are needed to demonstrate the presence of B1-receptor-mediated hypotension in the rat.