Bradykinin-induced dipsogenesis in captopril-treated rats.

The dipsogenic responsiveness to acute administration of the peptide, bradykinin, was studied in 4 groups of male Sprague-Dawley rats. All groups received captopril (35 mg/kg, IP) 15 minutes prior to the study. The first group then received saline (1 ml/kg, IP) while the remaining three groups received bradykinin at 50, 100 and 200 micrograms/kg, SC, respectively. The rats were placed alone into metabolic cages without food and given a preweighed bottle of tap water. Water intakes and urine outputs were then measured at 0.5, 1.0 and 2.0 hours thereafter. Bradykinin induced a dose-related increase in water intake but had no significant effect on urine output. To assess whether bradykinin might induce drinking by way of angiotensin II (AII) receptors, the AII receptor antagonist. Sar1, Ile8-AII (Sar, 300 and 600 micrograms/kg, SC) was administered to both bradykinin- (200 micrograms/kg, SC) and bradykinin plus captopril-treated (35 mg/kg, IP) groups of rats in a two-way ANOVA statistical design. Bradykinin again stimulated drinking in captopril-treated rats, but the drinking was not blocked significantly by administration of Sar. The results of this study indicate that blockade of the angiotensin I converting enzyme increases the half-life of bradykinin and unmasks its dipsogenic properties. The results suggest further that bradykinin does not appear to induce drinking via interaction with receptors for AII.