Laboratory Investigation

Kidney International (1982) 21, 466–470; doi:10.1038/ki.1982.47

Actions of angiotensin II on the isolated spontaneously hypertensive rat kidney

Thomas H Steele1, Jeanne H Gottstein1, Laura Challoner-Hue1 and Johnnie L Underwood1

1The Department of Medicine, University of Wisconsin, Madison, Wisconsin

Correspondence: T H Steele MD, Department of Medicine, University of Wisconsin, 470 North Charter Street, Madison, Wisconsin 53706, USA

Received 20 February 1981; Revised 24 July 1981.

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Abstract

Actions of angiotensin II on the isolated spontaneously hypertensive rat kidney. We studied the eflfects of angiotensin II (AII) on isolated spontaneously hypertensive rat (SHR) and Wistar-Kyoto control (WKY) kidneys utilizing a recirculating cell-free perfusate. Sufficient AII was infused to increase renal vascular resistance (RVR) by approximately 50%. When the perfusion pressure was allowed to increase with RVR during AII infusion, significant increases in the glomerular filtration rate (GFR), urine flow, and electrolyte excretion occurred in both the SHR and the WKY kidneys. However, when the increase in perfusion pressure was prevented, AII increased the GFR of SHR kidneys but had no effect on the GFR of WKY. In contrast to WKY, AII increased the GFR, urine flow, and sodium excretion of SHR kidneys as much at "normotensive" perfusion pressures as at "hypertensive" pressures. However, the "normotensive" perfusion pressures utilized in these studies were less than the blood pressure of the SHR in vivo. Accordingly, the response of SHR kidneys to AII was assessed when perfusion pressure was maintained constant at 160 torr. Under these conditions, AII did not elicit any further increases in GFR or changes in the electrolyte excretion. Results indicate that the renal perfusion pressure is a critical determinant of the renal responsiveness to AII and suggests that AII enhances renal function at perfusion pressures less than those customarily encountered in vivo.

Actions de l'angiotensine II sur le rein isolé de rats spontanément hypertendus. Nous avons étudié les effets de l'angiotensine II (AII) sur les reins isolés de rats spontanément hypertendus (SHR) et Wistar-Kyoto (WKY) en utilisant un perfusat recirculé dépourvu de cellules. Des quantités de AII suffisantes pour augmenter la résistance vasculaire rénale (RVR) de 50% ont été perfusées. Quand la pression de perfusion a été augmentée en même temps que RVR pendant la perfusion de AII, il a été observé des augmentations significatives du débit de filtration glomérulaire, du débit urinaire, de l'excrétion d'électrolytes, aussi bien chez SHR que WKY. Cependant, quand on a empêché l'augmentation de la pression de perfusion, AII a augmenté le débit de filtration glomérulaire des reins SHR, mais n'a pas eu d'effet sur celui des reins de WKY. A la différence de ce qui a été observé dans WKY, AII a augmenté le débit de filtration glomérulaire, le débit urinaire, l'excrétion de sodium des reins SHR autant aux pressions de perfusion "normotensives" qu'aux pressions de perfusion "hypertensives". Cependant, les pressions de perfusion "normotensives" utilisées dans ce travail étaient inférieures à la pression sanguine des animaux SHR in vivo. La réponse des reins SHR à AII a été évaluée quand la pression de perfusion a été maintenue constante à 160 torrs. Dans ces conditions, AII n'a pas entrainé d'augmentation supplémentaire du débit de filtration glomérulaire ou de modification de l'excrétion d'électrolytes. Les résultats indiquent que la pression de perfusion rénale est un déterminant critique de la réponse rénale à AII et suggère que AII augmente la fonction rénale chez SHR à des pressions de perfusion inférieures à celles habituellement recontrées in vivo.

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