Decreases in portal flow trigger a hepatorenal reflex to inhibit renal sodium and water excretion in rats: Role of adenosine

Abstract

The regulation of renal sodium and water excretion through a hepatorenal reflex activated by the changes in hemodynamics of the portal circulation has been suggested. We hypothesize that the changes in intrahepatic blood flow and flow-related intrahepatic adenosine are involved in the control of renal water and sodium excretion by triggering a hepatorenal reflex. Anesthetized rats were instrumented to monitor the systemic, hepatic, and renal circulation. A vascular shunt connecting the portal vein and central vena cava was established to allow for control of the portal venous blood flow (PVBF). Urine was collected from the bladder. The effects of decreased PVBF on renal water and sodium excretion were compared in normal and hepatic denervated rats. T he liver is involved in the regulation of renal excretion of sodium and water. [1][2][3][4][5] In this regard, the existence of a hepatorenal reflex to regulate urine production has been suggested. Lang et al. observed in a rat model that infusion of glutamine into the liver induced a hepatic and renal nerve-dependent reduction in renal glomerular filtration rate (GFR), renal plasma flow, and urine production. Other studies have also suggested that the activation of hepatic afferent nerves could result in the activation of renal sympathetic nerves to regulate renal function in health and diseases. [6][7][8][9][10] The changes in the hemodynamics of hepatic portal circulation have been considered as the major event in triggering the hepatorenal reflex. Theoretically, both increased portal veous blood pressure (PVP) and decreased portal venous blood flow (PVBF) could be the initial event that triggers the hepatorenal reflex. [3][4][5][6] Previous studies have been interpreted to indicate that PVP is the major event responsible for the triggering of the observed activation of the hepatorenal reflex. However, the maneuvers used in those studies to increase PVP unavoidably decreased or even stopped intrahepatic PVBF, leaving the issue unresolved. Moreover, an increased PVP as the trigger of the hepatorenal reflex would represent a positive-feedback mechanism, in which fluid retention would lead to an elevated PVP in healthy livers that would then result in more fluid retention. Little is known about the contribution of decreased intrahepatic PVBF in the regulation of renal water and sodium excretion.Thus, we tested the hypothesis that intrahepatic PVBF is involved in the regulation of renal water and sodium excretion. The experiments were performed in two different animal models: intrahepatic PVBF was reduced either by the portacaval shunt or by ligation of the superior mesenteric artery (SMA). The results revealed that renal water and sodium excretion were significantly decreased after reducing intrahepatic PVBF. The mechanism may relate to the flow-dependent accumulation of adenosine within the liver, triggering a hepatorenal reflex. Materials and Methods Surgical PreparationMale Sprague-Dawley rats weighing 260 to 300 g were maintained in the animal house under contro...

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