ABSTRACT
Bradykinin has been known to elicit a pressor effect when administered centrally, and a depressor effect when administered peripherally. The present study was aimed at investigating whether the blood pressure response to bradykinin is dependent on the endogenous generation of nitric oxide (NO). Effects of NG-nitro-L-arginine methyl ester (L-NAME) on the pressor and depressor responses to intracerebroventricularly and intravenously injected bradykinin (5nmol/rat), respectively, were examined in anesthetized rats. Neither the pressor response nor the depressor response was affected by acute parenteral treatment with L-NAME. The pressor and depressor effects of bradykinin were also noted in rats chronically supplemented with L-NAME in drinking water for 4 weeks. Bradykinin caused a relaxation of the isolated thoracic aorta in vitro, which was not affected in the presence of L-NAME. However, bradykinin failed to cause a relaxation of the aorta isolated from rats chronically treated with L-NAME. These findings suggest that endogenous generation of NO may not completely account for the blood pressure responses to bradykinin in rats.