Failure of high doses of Sar1-lle8-angiotensin II to abolish autoregulation of renal blood flow.

We used very high doses of a competitive inhibitor of angiotensin II to investigate the role of the intrarenal renin-angiotensin system in the autoregulation of renal blood flow. Studies were carried out in dogs in which the renin and prostaglandin systems were suppressed. The results of our studies indicate that angiotensin II is not a prime mediator of the autoregulation of renal blood flow in response to reduced perfusion pressure.