Anderson R J, Cronin R E, McDonald K M, Schrier R W
J Clin Invest. 1976 Oct;58(4):964-70. doi: 10.1172/JCI108550.
Clinical states with portal venous hypertension are frequently associated with impairment in renal hemodynamics and water excretion, as well as increased renin secretion. In the present investigation, portal venous pressure (PVP) was increased in anesthetized dogs undergoing a water diuresis. Renal arterial pressure was maintained constant in all studies. As PVP was increased from 6 to 20 mm Hg, decreases in cardiac output (2.5-2.0 liter/min, P less than 0.05) and mean arterial pressure (140-131 mm Hg, P less than 0.05) were observed. Increases in PVP were also associated with decreases in glomerular filtration rate (GFR, 40-31 ml/min, P less than 0.001), renal blood flow (RBF, 276-193 ml/min, P less than 0.001), and increases in renin secretion (232-939 U/min, P less than 0.025) in innervated kidneys. No significant change in either GFR or RBF and a decrease in renin secretion occurred with increases in PVP in denervated kidneys. To dissociate the changes in cardiac output and mean arterial pressure induced by increase PVP from the observed decreases in GFR and RBF, studies were performed on animals undergoing constriction of the thoracic inferior vena cava. In these studies, similar decreases in cardiac output and mean arterial pressure were not associated with significant changes in GFR or RBF. Increases in PVP also were associated with an antidiuresis as urine osmolality increased from 101 to 446 mosmol/kg H2O (P less than 0.001). This antidiuresis was significantly blunted but not abolished by acute hypophysectomy. In hypophysectomized animals, changes in free water clearance and urine flow were linearly correlated as PVP was increased. These studies indicate that increases in PVP result in decreases in GFR and RBF and increases in renin secretion mediated by increased renal adrenergic tone. Increased PVP is also associated with antidiuresis; this antidiuresis is mediated both by vasopressin release and by diminished tubular fluid delivery to the distal nephron.
门静脉高压的临床状态常伴有肾血流动力学和水排泄功能受损，以及肾素分泌增加。在本研究中，对处于水利尿状态的麻醉犬升高门静脉压力（PVP）。在所有研究中，肾动脉压保持恒定。当PVP从6mmHg升高至20mmHg时，观察到心输出量降低（从2.5降至2.0升/分钟，P<0.05）和平均动脉压降低（从140降至131mmHg，P<0.05）。PVP升高还与肾小球滤过率（GFR，从40降至31毫升/分钟，P<0.001）、肾血流量（RBF，从276降至193毫升/分钟，P<0.001）降低以及神经支配肾脏的肾素分泌增加（从232升至939U/分钟，P<0.025）有关。去神经支配的肾脏中，随着PVP升高，GFR或RBF均无显著变化，肾素分泌减少。为了将PVP升高引起的心输出量和平均动脉压变化与观察到的GFR和RBF降低区分开来，对下腔静脉胸段缩窄的动物进行了研究。在这些研究中，心输出量和平均动脉压的类似降低与GFR或RBF的显著变化无关。PVP升高还与抗利尿作用相关，此时尿渗透压从101升至446mosmol/kg H2O（P<0.001）。急性垂体切除可使这种抗利尿作用明显减弱但未消除。在垂体切除的动物中，随着PVP升高，自由水清除率和尿流量的变化呈线性相关。这些研究表明，PVP升高导致GFR和RBF降低以及肾素分泌增加，其机制是肾肾上腺素能张力增加。PVP升高还与抗利尿作用相关；这种抗利尿作用由血管加压素释放和远端肾单位肾小管液输送减少介导。
