Inhibition of prostaglandin and nitric oxide synthesis prevents cortisol-induced renal vasodilatation in sheep

Glucocorticoids increase renal blood flow (RBF) and glomerular filtration rate in many species, but the mechanisms involved are unclear We investigated whether cortisol-induced renal vasodilatation in conscious sheep depends on interactions with prostaglandins or angiotensin II. Intravenous infusion of cortisol (5 mg/h) for 5 h increased renal conductance (RC) by 1.06 +/- 0.24 ml . min(-1) . mmHg(-1) more than vehicle. During intrarenal infusion of indomethacin (0.25 mg . kg(-1) . h(-1)), the cortisol-induced increase in RC (0.28 +/- 0.21 ml . min(-1) . mmHg(-1)) was significantly reduced. The cortisol-induced rise in RBF (103 +/- 17 ml/min) was not significantly reduced by indomethacin treatment (76 +/- 9 ml/min). Combined intrarenal infusion of indomethacin (0.25 mg . kg(-1) . h(-1)) with N-omega-nitro-L-arginine (2.0 mg . kg(-1) . h(-1)), a nitric oxide synthase inhibitor, abolished the cortisol-induced increases in both RC and RBF. Inhibition of angiotensin II synthesis with intravenous captopril (40 mg/h) blocked the renal vasoconstrictor action of angiotensin I but did not inhibit the cortisol-induced increases in RBF and RC. This study provides evidence that nitric oxide and prostaglandins play a role in cortisol-induced renal vasodilatation but indicates that this response is independent of an interaction with angiotensin.