Actions of angiotensin II on the isolated spontaneously hypertensive rat kidney.
We studied the effects 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.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D005919:Glomerular Filtration Rate; D006973:Hypertension / Q000503:physiopathology* / Q000652:urine; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D051381:Rats; D012079:Renal Circulation / Q000187:drug effects; D012964:Sodium / Q000652:urine; D014655:Vascular Resistance / Q000187:drug effects
D000804:Angiotensin II; D012964:Sodium