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The interaction between the renin-angiotensin (RA) system and thromboxane A2 (TXA2) was examined in dogs, before and during the renal artery pressure (RAP) was decreased. Intrarenal arterial administration of a small dose of angiotensin II (AII) reduced renal blood flow (RBF) and glomerular filtration rate (GFR) in non-treated dogs when RAP was maintained at the normal level. When mean RAP was decreased to 60 mmHg by means of an aortic clamp, AII reduced RBF, but increased GFR up to 122% of the control value. In dogs pretreated by captopril, GFR decreased when RAP was reduced to 60 mmHg, while RBF was well maintained. However, with the administration of AII, RBF decreased markedly. By indomethacin pretreatment, GFR and RBF decreased during reduced RAP, and their reduction rates were accelerated with the administration of AII into the renal artery. By pretreatment with the thromboxane A2 synthetase inhibitor UK38485, the changes of RBF and GFR following AII infusion were similar to nontreated dogs at normal RAP, but during reduced RAP, AII infusion into the renal artery decreased GFR to 80% of the control value. The thromboxane B2 (TXB2) production by the renal cortex during reduced RAP increased to 2.7-fold that at normal RAP, but TXB2 production did not increase during reduced RAP in captopril pretreated dogs. These results suggest that the RA system and prostanoids, especially TXA2, are important factors for maintaining GFR at low RAP.

Mechanism of renin-angiotensin system and thromboxane A2 on maintenance of GFR during reduced renal perfusion pressure in dogs.