Role of prostaglandins in the increased vascular responsiveness to bradykinin in kidneys of spontaneously hypertensive rats.

Abstract

We examined the effects of arterial injections of bradykinin on perfusion pressure and output of PGE2 and 6-keto-PGF1 alpha in isolated kidneys of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). The kidneys were perfused with Krebs' bicarbonate buffer containing phenylephrine, both with and without indomethacin (1 microgram/mL). In kidneys perfused without indomethacin, bradykinin increased the output of PGE2 and 6-keto-PGF1 alpha in the kidneys of both WKY and SHR. Bradykinin also reduced perfusion pressure, indicative of renal vasodilation. This effect in the kidneys of SHR clearly exceeded that in the kidneys of WKY. The addition of indomethacin to the perfusion media suppressed the bradykinin-induced output of PGE2 and 6-keto-PGF1 alpha without altering the vasodilatory response to bradykinin in either SHR or WKY kidneys. Hence, the kidneys of SHR demonstrated an increased vasodilatory responsiveness to bradykinin irrespective of whether the peptide stimulated prostaglandin synthesis. We conclude that the augmented responsiveness of SHR kidneys to bradykinin-induced vasodilation cannot be attributed to enhanced expression of prostaglandin-mediated mechanisms of vasodilation.