Glucocorticoid-induced renal vasodilatation is mediated by a direct renal action involving nitric oxide

Abstract

Glucocorticoids increase renal blood flow (RBF) and glomerular filtration rate, but the mechanisms are unclear. We investigated whether the cortisol-induced increment in RBF is a direct renal action or secondary to its systemic effects and whether nitric oxide (NO) plays a role in this response. In conscious sheep, cortisol infused intravenously (5.0 mg/h) or into the renal artery (1.3 mg/h) for 5 h increased RBF by 66 +/- 8 and 53 +/- 11 ml/min, respectively. Plasma glucose was increased by intravenous cortisol (0.4 +/- 0.1 mmol/l) but not by intrarenal cortisol. Renal vein plasma cortisol levels were similar at the end of each infusion (193 +/- 31 intravenously; 151 +/- 25 nmol/l intrarena..