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

Abstract

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.