Akademik Veri Yönetim Sistemi
ARCHIVES INTERNATIONALES DE PHYSIOLOGIE DE BIOCHIMIE ET DE BIOPHYSIQUE, cilt.99, sa.6, ss.397-400, 1991 (SCI-Expanded)
Angiotensin II (A II) when given through the renal artery of the rabbit isolated perfused kidney elicited a concentration-dependent increase in perfusion pressure (PP) and urine flow (UF). Noradrenaline (NA) produced similar effect in PP but slightly not significantly increased UF. Addition of UK 38 485, a thromboxane A2. (TXA2)-synthetase inhibitor, to the bathing medium at the concentration of 10(-7)M caused a significant decrease in the pressor effect of A II but significantly enhanced UF. BM 13 177, a TXA2-receptor blocker, in the bathing medium (10(-6)M) produced identical effect in both PP and UF. The responses to NA were not significantly altered by both compounds. A II-induced enhancement of UF in presence of BM 13 177 was significantly lower than that obtained in presence of UK 38 485. These results were taken as an evidence that A II may increase the production of TXA2 in kidney probably originated from vascular bed or tubuli and part of the pressor effect of the peptide is due to this metabolite of arachidonic acid. Enhancement of UF following UK 38 485 is probably due to the shift of the synthesis toward E series of PGs. In addition this effect seems to be specific for A II since no such effect was seen with NA.