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Am J Physiol Regul Integr Comp Physiol 293: R1917-R1922, 2007. First published August 22, 2007; doi:10.1152/ajpregu.00180.2007
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RENAL HEMODYNAMICS AND CARDIORENAL INTEGRATION

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

Shereen M. Hamza and Susan Kaufman

Department of Physiology, University of Alberta, Edmonton, Alberta, Canada

Submitted 12 March 2007 ; accepted in final form 16 August 2007

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·min–1·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.

portal hypertension; spleen; renal sympathetic nerve activity



Address for reprint requests and other correspondence: S. Jacobs-Kaufman, 475 Heritage Medical Research Center, Univ. of Alberta, Edmonton, AB, Canada T6G 2S2 (e-mail: susan.jacobs{at}ualberta.ca)







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