Laboratory Investigation

Kidney International (1984) 26, 683–688; doi:10.1038/ki.1984.203

Pressure natriuresis and prostaglandin secretion by perfused rat kidney

Gilbert W Gleim1, Grace Kao-Lo1 and David L Maude1

1Department of Physiology, New York Medical College, Valhalla, New York

Correspondence: Dr D L Maude, Department of Physiology, Basic Sciences Building, New York Medical College, Valhalla, New York 10595, USA

Received 15 November 1983; Revised 5 March 1984.

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Abstract

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 (UNa V) 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-PGF1alpha, the regression lines relating GFR, FF, and UNa V 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.

Natriurèse d'hyperpression et sécrétion de prostaglandines par le rein de rat perfusé. Les reins de rat isolés répondent à des élévations de la pression de perfusion par une augmentation de débit de glomérulaire filtration (GFR), de la fraction de filtration (FF), et de l'excrétion de sodium (UNa V) et par une chute de la réabsorption fractionnelle de sodium (FRNa). Des corrélations linéaires significatives existent entre chacune de ces variables dépendantes et la pression de l'artère rénale (P). Chez les reins contrôles, la natriurèse d'hyperpression résulte à la fois d'une augmentation de la charge filtrée de sodium et d'une diminution de FRNa. Dans des reins traités par des doses d'indométhacine supprimant le relargage dans le perfusat de prostaglandine E2 (PGE2) et du métabolite de la prostacycline, la 6-céto-PGE1alpha, les droites de régression reliant GFR, FF, et UNa V à P sont décalées vers la droite. Ainsi les reins ayant une inhibition des prostaglandines ont besoin de pressions plus fortes que les reins contrôles pour maintenir des débits de filtration et d'excrétion sodée comparables. La résistance vasculaire rénale totale (RVR) est également plus élevée chez les reins inhibés. Ces résultats suggèrent que dans le rein de rat perfusé isolé, les prostaglandines permettent une natriurèse d'hyperpression en maintenant la dilatation artériolaire afférente. Leur inhibition conduit à une constriction afférente, laquelle augmente RVR, diminue FF et GFR, et réduit l'excrétion de sodium.

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