Pressure natriuresis and prostaglandin secretion by perfused rat kidney

Isolated rat kidneys respond to elevations of perfusion pressure with an increase in glomerular filtration rate (GFR), filtration fraction (FF), and sodium excretion (UNaV) and a fall in fractional sodium reabsorption (FRNa). Significant linear correlations exist between each of these dependent variables and the renal artery pressure (P). In control kidneys, pressure natriuresis is seen to result both from an increase in filtered sodium load and a decrease in FRNa. In kidneys treated with indomethacin in doses which curtail the release into the perfusate of prostaglandin E2 (PGE2) and the prostacyclin metabolite, 6-keto-PGF1 alpha, the regression lines relating GFR, FF, and UNaV to P are shifted to the right. Thus, prostaglandin-inhibited kidneys require higher pressures than control kidneys to maintain comparable rates of filtration and sodium excretion. Total renal vascular resistance (RVR) is also higher in inhibited kidneys. These findings suggest that in the isolated perfused rat kidney, prostaglandins promote pressure natriuresis by maintaining afferent arteriolar dilation. Their inhibition leads to afferent constriction, which raises RVR, lowers FF and GFR, and reduces sodium excretion.