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

Abstract

Hamza SM, Kaufman S. Effect of mesenteric vascular congestion on reflex control of renal blood flow. Am J Physiol Regul Integr Comp Physiol 293: R1917-R1922, 2007. First published August 22, 2007; doi:10.1152/ajpregu.00180.2007.-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 Ϯ 0.1 to 13.2 Ϯ 0.1 mmHg; n ϭ 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 (Ϫ1.2 Ϯ 0.2 ml/min; n ϭ 9) that was attenuated by renal denervation (Ϫ0.5 Ϯ 0.1 ml/min; n ϭ 6), splenic denervation (Ϫ0.2 Ϯ 0.1 ml/min; n ϭ 11), celiac ganglionectomy (Ϫ0.3 Ϯ 0.1 ml/min; n ϭ 9), and splenectomy (Ϫ0.5 Ϯ 0.1 ml/min; n ϭ 6). Caudal occlusion induced a significantly smaller fall in RBF (Ϫ0.5 Ϯ 0.1 ml/min; n ϭ 9), which was not influenced by renal denervation (Ϫ0.2 Ϯ 0.2 ml/min; n ϭ 6), splenic denervation (Ϫ0.1 Ϯ 0.1 ml/min; n ϭ 7), celiac ganglionectomy (Ϫ0.1 Ϯ 0.3 ml/min; n ϭ 8), or splenectomy (Ϫ0.3 Ϯ 0.1 ml/min; n ϭ 7). Renal arterial conductance fell only in intact animals subjected to rostral occlusion (Ϫ0.007 Ϯ 0.002 ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 ). This was accompanied by increases in splenic afferent nerve activity (15.0 Ϯ 3.5 to 32.6 Ϯ 6.2 spikes/s; n ϭ 7) and renal efferent nerve activity (32.7 Ϯ 5.2 to 39.3 Ϯ 6.0 spikes/s; n ϭ 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.

Regional Blood Flow Distribution and Oxygen Metabolism During Mesenteric Ischemia and Congestion

“…Previously, we and others have demonstrated an increase of 200% to 300% in the SMV hydrostatic pressure in animals subjected to portal or mesenteric vein occlusion [9,10]. The increase of hematocrit in the mesenteric vein in the SMVO group (66.4% 6 0.9% versus 34.3% 6 1.5%, P < 0.05) during the ''ischemic'' period (II-45), and the higher wall congestion score observed during histological evaluation (2.8 6 0.2 versus 0.8 6 0.2, P < 0.05), corroborate the fluid sequestration hypothesis.…”

Importance of Venous Congestion for Worsening of Renal Function in Advanced Decompensated Heart Failure

“…Other studies indicated that temporary renal vein compression resulted in reduced sodium excretion, reduced GFR and reduced renal blood flow (16–18). Increased CVP also causes an increase in renal interstitial pressure, which might lead to a hypoxic state of the renal parenchyma similar to the mechanism by which hepatic congestion leads to liver dysfunction in heart failure (19–25). In addition, our group recently provided some mechanistic data to suggest the contributions of raised intra-abdominal pressure caused by visceral edema or ascites in this pathophysiology (26).…”

Effect of Right Ventricular Function and Venous Congestion on Cardiorenal Interactions During the Treatment of Decompensated Heart Failure

“…These models demonstrate rapid and profound decreases in renal blood flow, glomerular filtration rate, ultrafiltration coefficient, and increased sodium avidity after partial balloon occlusion or external compression of the renal veins, inferior vena cava, or the veins of specific abdominal organs (13,19–24). These effects are rapidly reversed with relief of the venous obstruction and can be significantly attenuated with alpha receptor blockade or denervation of the kidney (19–20,23–25). Additionally, recent reports have confirmed that venous congestion is a relevant factor influencing renal function in humans (12,26,27).…”