Sympathetic nervous system in the loss of autoregulation in acute renal failure.

The responsiveness of the renal vascular system was investigated in uninephrectomized Sprague-Dawley rats in which acute renal failure had been induced by norepinephrine. The animals were studied at 1' and 3 wk after norepinephrine infusion. Uninephrectomized littermates served as controls. Compared with controls, there was an absence of renal blood flow autoregulation in 1-wk acute renal failure that returned in part by 3 wk. In 1-wk rats there was a marked increase, rather than decrease, in renovascular resistance as renal perfusion pressure was decreased. The renal vasculature was significantly less responsive in 1-wk rats than in control or 3-wk animals when acetylcholine, angiotensin II, or norepinephrine was infused into the renal artery at minimal vasoactive doses (all P less than 0.01). Paradoxically, renal vasoconstriction in response to renal nerve stimulation was greater in 1-wk than in 3-wk and control rats (P less than 0.01) and was not inhibited by renal artery infusion of phenoxybenzamine. Renal denervation significantly improved renal blood flow autoregulation in 1-wk animals (P less than 0.001) and completely abolished the increase in renovascular resistance as renal perfusion pressure was lowered. No effects of renal denervation on renal blood flow autoregulation were seen in control and 3-wk rats. It is concluded that renovascular responses to neurohumoral stimuli are aberrant in acute renal failure. The loss of renal blood flow autoregulation is related to an increased renovascular resistance that is due to increased activity of non-alpha-adrenergic mechanisms of the autonomic nervous system.