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

Abstract

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.

AKI Associated with Cardiac Surgery

“…On the basis of two small studies, it seems that higher perfusion pressures may improve renal function during cardiopulmonary bypass but do not affect postoperative function (120,124). The existence of CKD as well as chronic hypertension may affect the ideal mean arterial pressure, because renal injury seems to be accompanied by a loss of autoregulation (125,126). Some data suggest that off-pump coronary artery bypass (OPCAB) surgery reduces the incidence of perioperative AKI (127-131); however, this finding is not universal (131,132).…”

Diagnosis and Treatment of Acute Tubular Necrosis

“…Furthermore, paradoxical renal vasoconstriction occurs at low mean arterial pressure (64,65). In addition, animal models have demonstrated increased intrinsic renal vascular tone and increased sensitivity to vasoconstrictive stimuli that contribute to impaired GFR (66,67). Thus, either mild or severe decreases in blood pressure due to volume depletion, dialysis, sepsis, cardiac dysfunction, anesthesia, or antihypertensive medications can further decrease renal perfusion and lead to recurrent ischemic injury.…”

Smooth muscle calcium and endothelium-derived relaxing factor in the abnormal vascular responses of acute renal failure.

“…19:217A.). cent years, the tubular abnormalities have been intensively studied (5)(6)(7)(8), while the vascular abnormalities have received less attention (9,10). It has become clear, however, that an ischemic renal injury sufficient to cause reversible ARF is associated with abnormal renovascular reactivity in both the dog (10) and rat (9).…”

“…cent years, the tubular abnormalities have been intensively studied (5)(6)(7)(8), while the vascular abnormalities have received less attention (9,10). It has become clear, however, that an ischemic renal injury sufficient to cause reversible ARF is associated with abnormal renovascular reactivity in both the dog (10) and rat (9). Paradoxical vasoconstriction to a reduction in renal perfusion pressure (RPP) in the normal autoregulatory range, hypersensitivity to renal nerve stimulation (RNS), and loss of the renal vasodilatory effect of acetylcholine have been described (9).…”

“…It has become clear, however, that an ischemic renal injury sufficient to cause reversible ARF is associated with abnormal renovascular reactivity in both the dog (10) and rat (9). Paradoxical vasoconstriction to a reduction in renal perfusion pressure (RPP) in the normal autoregulatory range, hypersensitivity to renal nerve stimulation (RNS), and loss of the renal vasodilatory effect of acetylcholine have been described (9). These vascular phenomena have been proposed to provide a potential explanation for the clinical observation that fresh tubular necrotic lesions have been demonstrable in renal tissues as late as 4 wk after the overt clinical episode causing the ARF (1 1).…”