Role of vasopressin in impaired water excretion in conscious rats with experimental cirrhosis

Linas, Stuart L.; Anderson, Robert J.; Guggenheim, Stephen; Robertson, Gary; Berl, Tomás; Dickmann, David

doi:10.1038/ki.1981.119

Cited by 76 publications

(27 citation statements)

References 38 publications

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“…Thus, water retention seems to exceed the sodium retention. Consistent with this, the changes in AQP2 all are consistent with increased vasopressin levels (2,23). Arguably, this means that the sodium retention is appropriate to retain plasma osmolality.…”

Section: Increased Apical Targeting Of Enac Subunits In CCL 4 -Treatesupporting

confidence: 63%

“…The purposes of this study, therefore, were (1) to examine whether there are changes in the protein abundance and/or apical targeting of ENaC subunits in kidneys of rats with CCl 4 -induced liver cirrhosis, (2) to examine whether there are changes in the protein abundance of 11␤HSD2, (3) to examine whether there are changes in the protein abundance of other renal sodium transporters along the renal tubules (type 3 Na/H exchanger [NHE3] and Na-K-2Cl co-transporter [NKCC2]), and (4) to examine whether these changes are associated with changes in the urinary sodium excretion.…”

mentioning

confidence: 99%

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Increased Apical Targeting of Renal Epithelial Sodium Channel Subunits and Decreased Expression of Type 2 11β-Hydroxysteroid Dehydrogenase in Rats with CCl4-Induced Decompensated Liver Cirrhosis

Kim¹,

Schou²,

Peters³

et al. 2005

Journal of the American Society of Nephrology

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It was hypothesized that dysregulation of renal epithelial sodium channel (ENaC) subunits and/or 11␤-hydroxysteroid dehydrogenase (11␤HSD2) may play a role in the increased sodium retention in liver cirrhosis (LC). Experimental LC was induced in rats by CCl 4 (1 ml/kg, intraperitoneally, twice a week) for 12 wk (protocol 1) or for 11 wk (protocol 2). In both protocols, one group of rats with cirrhosis showed significantly decreased urinary sodium excretion and urinary Na/K ratio (group A), whereas a second group exhibited normal urinary sodium excretion (group B) compared with controls, even though extensive ascites was seen in both groups of rats with cirrhosis. In group A, protein abundance of ␣-ENaC was unchanged, whereas ␤-ENaC abundance was decreased in the cortex/outer stripe of outer medulla compared with controls. The ␥-ENaC underwent a complex change associated with increased abundance of the 70-kD band with a concomitant decrease in the main 85-kD band, corresponding to an aldosterone effect. In contrast, no changes in the abundance of ENaC subunit were observed in group B. Immunoperoxidase microscopy revealed an increased apical targeting of ␣-, ␤-, and ␥-ENaC subunits in distal convoluted tubule (DCT2), connecting tubule (CNT), and cortical and medullary collecting duct segments in group A but not in group B. Immunolabeling intensity of 11␤HSD2 in the DCT2, CNT, and cortical collecting duct was significantly reduced in group A but not in group B, and this was confirmed by immunoblotting. In conclusion, increased apical targeting of ENaC subunits combined with diminished abundance of 11␤HSD2 in the DCT2, CNT, and cortical collecting duct is likely to play a role in the sodium retaining stage of liver cirrhosis.

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Section: Increased Apical Targeting Of Enac Subunits In CCL 4 -Treatesupporting

confidence: 63%

mentioning

confidence: 99%

Increased Apical Targeting of Renal Epithelial Sodium Channel Subunits and Decreased Expression of Type 2 11β-Hydroxysteroid Dehydrogenase in Rats with CCl4-Induced Decompensated Liver Cirrhosis

Kim¹,

Schou²,

Peters³

et al. 2005

Journal of the American Society of Nephrology

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“…Furthermore, Brattleboro rats with experimental cirrhosis, a strain with a congenital deficiency of VP, do not develop an impairment in water excretion. 88 Administration of a V 2 -receptor peptide antagonist restores the ability to excrete water in cirrhotic rats. 89 This hypersecretion of VP is caused by an increased synthesis because the hypothalamic VP mRNA content is increased in cirrhotic rats.…”

Section: Water Retention and Cirrhosismentioning

confidence: 99%

Hyponatremia in cirrhosis: From pathogenesis to treatment

et al. 1998

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“…Animal studies support these clinical observations, with a linear relationship between plasma vasopressin concentration and water excretion observed in rodent models of cirrhosis [26]. Furthermore, Battleboro rats, which have a congenital vasopressin deficiency, do not develop impaired water handling with carbon tetrachlorideinduced liver cirrhosis [27].…”

Section: Pathophysiologymentioning

confidence: 85%

Therapeutic role of vasopressin receptor antagonism in patients with liver cirrhosis

et al. 2003

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Vasopressin, or antidiuretic hormone, is a peptide hormone that is released from the posterior pituitary gland in response to changes in blood pressure and plasma osmolality. The main pathophysiological states associated with high plasma vasopressin concentrations are cirrhosis, cardiac failure and syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Pharmacological treatments for disorders of excess vasopressin secretion have been limited. However, oral bio-available selective and non-selective V(1) and V(2) receptor antagonists have recently become available for clinical use. Water retention in cirrhosis is a common problem, leading to ascites, peripheral oedema and hyponatraemia. Raised plasma vasopressin concentrations and decreased delivery of glomerular filtrate are believed to be the most important factors in the development of water retention. V(2) receptor antagonists are aquaretic agents that promote water excretion and improve hyponatraemia. Their potential role in cirrhosis has been examined in a number of recent studies that have shown increased free water clearance and serum sodium concentrations with few adverse effects. V(2) receptor antagonists represent a novel and promising new class of agent that may have major clinical utility in the treatment of patients with liver cirrhosis.

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Role of vasopressin in impaired water excretion in conscious rats with experimental cirrhosis

Cited by 76 publications

References 38 publications

Increased Apical Targeting of Renal Epithelial Sodium Channel Subunits and Decreased Expression of Type 2 11β-Hydroxysteroid Dehydrogenase in Rats with CCl4-Induced Decompensated Liver Cirrhosis

Increased Apical Targeting of Renal Epithelial Sodium Channel Subunits and Decreased Expression of Type 2 11β-Hydroxysteroid Dehydrogenase in Rats with CCl4-Induced Decompensated Liver Cirrhosis

Hyponatremia in cirrhosis: From pathogenesis to treatment

Therapeutic role of vasopressin receptor antagonism in patients with liver cirrhosis

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