4.3 Article

Effect of mesenteric vascular congestion on reflex control of renal blood flow

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AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00180.2007

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portal hypertension; spleen; renal sympathetic nerve activity

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Portal hypertension initiates a splenorenal reflex, whereby increases in splenic afferent nerve activity and renal sympathetic nerve activity cause a decrease in renal blood flow (RBF). We postulated that mesenteric vascular congestion similarly compromises renal function through an intestinal-renal reflex. The portal vein was partially occluded in anesthetized rats, either rostral or caudal to the junction with the splenic vein. Portal venous pressure increased (6.5 +/- 0.1 to 13.2 +/- 0.1 mmHg; n = 78) and mesenteric venous outflow was equally obstructed in both cases. However, only rostral occlusion increased splenic venous pressure. Rostral occlusion caused a fall in RBF ( - 1.2 +/- 0.2 ml/min; n = 9) that was attenuated by renal denervation ( - 0.5 +/- 0.1 ml/min; n = 6), splenic denervation ( - 0.2 +/- 0.1 ml/min; n = 11), celiac ganglionectomy ( - 0.3 +/- 0.1 ml/min; n = 9), and splenectomy ( - 0.5 +/- 0.1 ml/min; n = 6). Caudal occlusion induced a significantly smaller fall in RBF ( - 0.5 +/- 0.1 ml/min; n = 9), which was not influenced by renal denervation ( - 0.2 +/- 0.2 ml/min; n = 6), splenic denervation ( - 0.1 +/- 0.1 ml/min; n = 7), celiac ganglionectomy ( - 0.1 +/- 0.3 ml/min; n = 8), or splenectomy ( - 0.3 +/- 0.1 ml/min; n = 7). Renal arterial conductance fell only in intact animals subjected to rostral occlusion ( - 0.007 +/- 0.002 ml center dot min(-1)center dot mmHg(-1)). This was accompanied by increases in splenic afferent nerve activity (15.0 +/- 3.5 to 32.6 +/- 6.2 spikes/s; n = 7) and renal efferent nerve activity ( 32.7 +/- 5.2 to 39.3 +/- 6.0 spikes/s; n = 10). In animals subjected to caudal occlusion, there were no such changes in renal arterial conductance or splenic afferent/renal sympathetic nerve activity. We conclude that the portal hypertension-induced fall in RBF is initiated by increased splenic, but not mesenteric, venous pressure, i.e., we did not find evidence for intestinal-renal reflex control of the kidneys.

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