Autoregulation of renal and splanchnic blood flow following infra-renal aortic clamping is mediated by nitric oxide and vasodilator prostanoids

Objective. This study examines the hypothesis that nitric oxide and vasodilator prostanoids contribute to the autoregulation of renal artery and superior mesenteric artery (SMA) blood flow following infra-renal aortic clamping. Experimental design. Renal and SMA artery blood flow were measured in anesthetized rats. The rats received bolus injection of saline carrier, L-NAME (25 mg/kg) or indomethacin (15 mg/kg) prior to sham or infra-renal aortic occlusion. In vivo blood flow was measured 1, 30 and 60 minutes during aortic occlusion and 1, 30, and 60 minutes following release of the aortic cross clamp. Results. Aortic occlusion transiently increased SMA blood now but did not alter renal artery blood flow. Aortic clamp release resulted in a 40% decrease in both SMA and renal artery blood flow, L-NAME or indomethacin pretreatment decreased both SMA and renal artery blood flow at 60 minutes following infra-renal aortic occlusion. Indomethacin decreased SMA blood now at 1 minute following unclamping of the aorta and L-NAME decreased SMA blood flow at 30 and 60 minutes following aortic clamp release. Both L-NAME and indomethacin markedly decreased renal artery blood flow at all time periods following aortic clamp release. Conclusions. These data suggest that renal and splanchnic vascular beds utilize endogenous vasodilator eicosanoids and nitric oxide to maintain blood now during cross clamping and unclamping of the infra-renal aorta.