Angiotensin converting enzyme inhibition (ACEI) with captopril has been shown to increase water intake and urine output in rats but the mechanism is unknown. ACEI is known to impair the conversion of angiotensin I to angiotensin II (ANG II), a dipsogenic hormone, and to impair the degradation of bradykinin. The goal of this study was to examine the role of bradykinin in the polydipsia and polyuria associated with ACEI. Water intake, food intake, and urine output were monitored in male Sprague-Dawley rats for the initial two days of study. Rats were then divided into 4 study groups: 1) control rats receiving plain chow with ad libitum water (CTL); 2) captopril treatment 20 mg/kg/day in ground rat chow with ad libitum drinking water (CPT); 3) captopril treatment with water intake limited to the daily volume consumed in the baseline period (CPT-LIM); and 4) captopril treatment with ad libitum water intake plus Q8h injection of the bradykinin antagonist B-9430 in the final 24h of study (CPT-BKI). A water balance study was performed in the final 24h of study. Mean arterial pressure and 24h creatinine clearance were assessed. CPT rats consumed more water (40 ± 2 vs. 29 ± 2 ml/day, p<0.01) and produced more urine (20 ± 3 vs. 8 ± 1 ml/day, p<0.001) as compared to CTL. Urine osmolality (UOsm) was decreased in CPT rats (1277 ± 288 vs. 2415 ± 384 mOsm/kg H₂O, p<0.05) versus CTL. Inner medulla aquaporin-2 (AQP2) protein abundance was also decreased in CPT rats (52 ± 7 vs. 100 ± 12% control mean, p<0.05). These findings were reversed in CPT-LIM rats (water intake 29 ± 2 ml/day; urine output 8 ± 2 ml/day; UOsm 2547 ± 183 mOsm/kg H₂O; AQP2 112 ± 2% control mean; all pNS vs. CTL), suggesting captopril-induced primary polydipsia. CPT-BKI rats demonstrated parameters similar to CTL despite ad libitum water intake (water intake 31 ± 1 ml/day; urine output 8 ± 1 ml/day; UOsm 1866 ± 83 ml/day; AQP2 95 ± 10% control mean; all pNS vs. CTL). Mean arterial pressure, 24h creatinine clearance, and inner medulla protein abundance of AQP3 or AQP4 did not differ between groups. We conclude that ACEI with captopril induces primary polydipsia despite impaired production of the dipsogen ANG II and that this primary increase in water intake is likely the cause of the decreased protein abundance of inner medulla AQP2. Furthermore, this dipsogenic effect was reversed by antagonism of bradykinin, thus implicating this hormone in thirst regulation in the rat.