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

Cronin, Robert E.; McDonald, Keith M.; Schrier, Robert W.

doi:10.1172/jci108550

Cited by 70 publications

(29 citation statements)

References 26 publications

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“…In agreement with these results, it has been reported that an acute increase in portal venous pressure due to the extraluminal obstruction of the portal vein causes a reduction of arterial blood pressure, cardiac output, renal blood flow, and glomerular filtration rate (LIANG, 1971;LEVY, 1974;ANDERSON et al, 1976). When portal venous pressure exceeded appoximately 30 cmH2O, arterial blood pressure significantly fell and glomerular filtration rate was reduced significantly (LEVY, 1974;ANDERSON et al, 1976). LEVY (1974) reported, in addition, that portal venous hypertension did not appear to modify renal function unless systemic hypotension coexisted.…”

Section: Discussionsupporting

confidence: 79%

“…It was reported that increases in renal sympathetic activity produced increases in renin secretion from the kidney (KOYAMA et al, 1980(KOYAMA et al, , 1981AMMONS et a!., 1982). ANDERSON et al (1976) also demonstrated that increases in portal venous pressure resulted in increases in renin secretion mediated by activation of renal symapthetic tone.…”

Section: Discussionmentioning

confidence: 96%

“…Thereby, the systemic hypotension itself due to portal hypertension could produce an alteration of renal function induced by either neural or humoral factors. LIANG (1971) and ANDERSON et al (1976) demonstrated that chemical or surgical denervation of renal nerves abolished the renal response to the elevation of portal ^venous pressure. Therefore, they suggested that decreases in renal blood flow and glomerular filtration rate due to portal hypertension might be a result of neural reflex activity.…”

Section: Discussionmentioning

confidence: 99%

“…One possible explanation of this finding is that afferent nerves from the portal venous vascular wall may be stimulated by an increase in the portal venous pressure, leading to excitatory renal sympathetic activity. ANDERSON et al (1976) indicated that there appeared to be a hepato-renal reflex in which increased portal venous pressure initiated a sympathetically mediated decrease in renal blood flow. Recently, NIIJIMA (1977) reported an increase in sympathetic afferent activity of hepatic nerves located in or near the venous wall of the portal vein during the portal hypertension in an isolated liver preparation .…”

Section: Discussionmentioning

confidence: 99%

“…Such a reflex has been demonstrated experimentally by increasing the portal venous pressure and observing the reduction of systemic blood pressure, renal blood flow, as well as glomerular filtration rate (LIANG, 1971;LEVY, 1974;ANDERSON et al, 1976). LIANG (1971) and ANDERSON et al (1976) reported that the renal hemodynamic response to increased portal vein pressure was prevented by renal nerve denervation, suggesting that increases in sympathetic nerve activity caused a decrease in renal perfusion flow. In these reports, however, they have not shown to what extent the functions of the arterial or cardiopulmonary baroreceptor systems are contributing to these hepato-renal reflexes.…”

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confidence: 98%

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Reflex renal vasoconstriction on portal vein distension.

et al. 1986

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The present experiments were designed to study effects of neural control mechanisms on renal sympathetic nerve activity during acute portal vein distension in anesthetized dogs. Following the inflation of a balloon placed into the main portal vein of animals with the neuraxis intact (intact group), portal vein pressure at a site of the splanchnic regions increased significantly. Mean blood pressure (MBP) fell significantly and then renal vascular resistance (RVR) increased significantly in parallel with changes in portal venous pressure. In animals with sinoaortic denervation (SAD group), changes in portal venous pressure during the inflation of a balloon did not differ from the intact group. However, decreases in MBP in the SAD group were greater than that in the intact group, and sinoaortic denervation did not alter increases in RVR. In animals with both sinoaortic denervation and cervical vagotomy (vagotomy group), portal vein distension produced more profound hypotension, and significant increases in RVR occurred. This increase in RVR, however, was abolished by renal nerve denervation. The results of the present study indicate that increases in RVR during the portal vein distension, which is associated with systemic hypotension, may be mediated by an activation of efferent sympathetic renal nerves and modified by at least two neural reflex mechanisms such as carotid sinus baroreceptors and cardiopulmonary baroreceptors. In addition, local reflex systems such as stretch receptors in the venous wall of the portal vein may be involved in excitatory response to renal sympathetic nerve, leading to renal vasoconstriction, during the portal vein distension.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

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Reflex renal vasoconstriction on portal vein distension.

et al. 1986

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Pathogenesis of Hyponatremia: The Role of Arginine Vasopressin

Ishikawa¹,

Schrier²

2005

Ascites and Renal Dysfunction in Liver Disease

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A Comparison of Acute Reversible Pre- and Postsinusoidal Portal Hypertension on Salt and Water Retention in the Dog

et al. 1982

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To define the relationship between portal hypertension and renal excretion of salt and water, two acute animal models of portal hypertension were investigated. In both models, it was necessary for systemic and renal hemodynamics to remain unchanged during the creation of portal hypertension so as to eliminate the effects of change in these parameters on renal excretion.In eight dogs, portal hypertension was induced by controlled tightening of a ligature around the superior hepatic vein and changes in hemodynamics were prevented by controlled i.v. titration with canine plasma. Rises in portal pressure 9.3 k 2.6 to 15.6 f 2.3 cm HZO were associated with significant decreases in urine volume 1.57 k 0.53 to 0.66 k 0.21 ml per min (p < 0.05) and urinary sodium excretion 1340 & 82 to 145 k 76 mEq per min (p < 0.05)]. In contrast, similar experiments in five dogs in which the portal vein was partially ligated with increases in portal pressure from 8.3 f 0.6 to 18.6 & 0.5 cm HzO resulted in no change in urinary volume or sodium excretion.Acute reversible portal hypertension induced by hepatic vein constriction is associated with acute reversible retention of water and salt in the absence of changes in renal blood flow and creatinine clearance which only occur when the liver is involved and not with portal vein constriction.Many patients with advanced cirrhosis develop renal sodium retention and ascites. In the past, this sodium retention has been thought to be the result of fluid loss into the ascitic "third space" secondary to increased hydrostatic pressure in the hepatic sinusoids and splanchnic capillaries with a decrease in effective circulatory volume and appropriate alteration in renin and aldosterone secretion. Although plasma volume measurements in cirrhotics are actually normal or slightly elevated, it has been postulated that the ('central'' or nonsplanchnic component is decreased and the splanchnic component increased. Lieberman, in 1969, presented data from studies in human cirrhosis which suggested that renal sodium retention actually preceded the development of ascites, and was in fact, a contributing factor in the development of ascites (1). He postulated the existence of some hepatic factors which altered renal sodium handling independent of volume changes and the reninaldosterone regulatory mechanisms.

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

Cited by 70 publications

References 26 publications

Reflex renal vasoconstriction on portal vein distension.

Reflex renal vasoconstriction on portal vein distension.

Pathogenesis of Hyponatremia: The Role of Arginine Vasopressin

A Comparison of Acute Reversible Pre- and Postsinusoidal Portal Hypertension on Salt and Water Retention in the Dog

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