Actions of angiotensin II on the isolated spontaneously hypertensive rat kidney.

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 160torr. 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 isole de rats spontanement hypertendus. Nous avons etudie les effets de l'angiotensine II (AII) sur les reins isoles de rats spontanement hypertendus (SHR) et Wistar-Kyoto (WKY) en utilisant un perfusat recircule depourvu de cellules. Des quantites de AII suffisantes pour augmenter la resistance vasculaire renale (RVR) de 50% ont ete perfusees. Quand la pression de perfusion a ete augmentee en meme temps que RVR pendant la perfusion de AII, il a ete observe des augmentations significatives du debit de filtration glomerulaire, du debit urinaire, de l'excretion d'electrolytes, aussi bien chez SHR que WKY. Cependant, quand on a empeche l'augmentation de la pression de perfusion, AII a augmente le debit de filtration glomerulaire des reins SHR, mais n'a pas eu d'effet sur celui des reins de WKY. A la difference de ce qui a ete observe dans WKY, AII a augmente le debit de filtration glomerulaire, le debit urinaire, l'excretion de sodium des reins SHR autant aux pressions de perfusion "normotensives" qu'aux pressions de perfusion "hypertensives". Cependant, les pressions de perfusion "normotensives" utilisees dans ce travail etaient inferieures a la pression sanguine des animaux SHR in vivo. La reponse des reins SHR a AII a ete evaluee quand la pression de perfusion a ete maintenue constante a 160torrs. Dans ces conditions, AII n'a pas entraine d'augmentation supplementaire du debit de filtration glomerulaire ou de modification de l'excretion d'electrolytes. Les resultats indiquent que la pression de perfusion renale est un determinant critique de la reponse renale a AII et suggere que AII augmente la fonction renale chez SHR a des pressions de perfusion inferieures a celles habituellement recontrees in vivo.