Mechanisms of portal hypertension induced alterations in renal hemodynamics, renal water excretion, and renin secretion

R. J. Anderson, R. E. Cronin, K. M R W McDonald andSchrier

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61 Scopus citations


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, decrease in cardiac output (2.5-2.0 liter/min, P < 0.05) and mean arterial pressure (140-131 mm Hg, P < 0.05) were observed. Increases in PVP were also associated with decreases in glomerular filtration rate (GFR, 40-31 ml/min, P < 0.001), renal blood flow (RBF, 267-193 ml/min, P < 0.001), and increases in renin secretion (232-939 U/min, P < 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 increased 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 < 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.

Original languageEnglish (US)
Pages (from-to)964-970
Number of pages7
JournalJournal of Clinical Investigation
Issue number4
StatePublished - 1976

ASJC Scopus subject areas

  • Medicine(all)


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