Collecting duct function in liver cirrhotic rats with early sodium retention

Jonassen, Thomas E. N.; Heide, Andreas; Janjua, Nadeem Rezaq; Christensen, Sten

doi:10.1046/j.1365-201x.2002.00993.x

Cited by 6 publications

(4 citation statements)

References 20 publications

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“…Na ϩ ,K ϩ -ATPase was not altered in the medullary and cortical thick ascending limb of Henle's loop (MTAL and CTAL), although this nephron segment was proposed as a main site of sodium retention in BDL rats. 40,41 Na ϩ ,K ϩ -ATPase activity was decreased in the proximal tubule of BDL mice, confirming previous findings in cirrhotic BDL rats showing decreased proximal sodium reabsorption and expression of Na ϩ ,K ϩ -ATPase and of the sodium proton exchanger, the main apical sodium transporter in proximal tubule. 3 The third aim was to evaluate the role of hyperaldosteronemia in sodium retention in cirrhosis.…”

Section: Discussionsupporting

confidence: 78%

“…Although several reports in experimental models of cirrhosis show that sodium retention originates along the aldosterone-sensitive nephron segments, 29,32,[34][35][36][37][38][39] other reports concluded to the thick ascending limb of Henle's loop as the main site of sodium retention in rat models. 40,41 The present study aimed at (1) localizing the site of sodium retention along the nephron, and (2) at determining the role of aldosterone and MR in sodium retention. We therefore developed a mouse model of cholestatic cirrhosis: sodium-and potassium-dependent adenosine triphosphatase (Na ϩ ,K ϩ -ATPase) activity was used as a marker of sodium reabsorption, and the role of aldosterone and MR was evaluated in corticosteroid-clamped animals.…”

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confidence: 99%

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Sodium retention and ascites formation in a cholestatic mice model: Role of aldosterone and mineralocorticoid receptor?

et al. 2007

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Renal sodium retention in experimental liver cirrhosis originates from the distal nephron sensitive to aldosterone. The aims of this study were to (1) determine the exact site of sodium retention along the aldosterone-sensitive distal nephron, and (2) to evaluate the role of aldosterone and mineralocorticoid receptor activation in this process. Liver cirrhosis was induced by bile duct ligation in either adrenalintact or corticosteroid-clamped mice. Corticosteroid-clamp was achieved through adrenalectomy and corticosteroid supplementation with aldosterone and dexamethasone via osmotic minipumps. 24-hours renal sodium balance was evaluated in metabolic cages. Activity and expression of sodiumand potassium-dependent adenosine triphosphatase were determined in microdissected segments of nephron. Within 4-5 weeks, cirrhosis induced sodium retention in adrenal-intact mice and formation of ascites in 50% of mice. At that time, sodium-and potassium-dependent adenosine triphosphatase activity increased specifically in cortical collecting ducts. Hyperaldosteronemia was indicated by increases in urinary aldosterone excretion and in sgk1 (serum-and glucocorticoid-regulated kinase 1) mRNA expression in collecting ducts. Corticosteroid-clamp prevented induction of sgk1 but not cirrhosis-induced sodium retention, formation of ascites and stimulation of sodium-and potassiumdependent adenosine triphosphatase activity and expression (mRNA and protein) in collecting duct. These findings demonstrate that sodium retention in cirrhosis is independent of hyperaldosteronemia and of the activation of mineralocorticoid receptor. Conclusion: Bile duct ligation in mice induces cirrhosis which, within 4-5 weeks, leads to the induction of sodium-and potassium-dependent adenosine triphosphatase in cortical collecting ducts, to renal sodium retention and to the formation of ascites. Sodium retention, ascites formation and induction of sodium-and potassium-dependent adenosine triphosphatase are independent of the activation of mineralocorticoid receptors by either aldosterone or glucocorticoids. (HEPATOLOGY 2007;46:173-179.) See Editorial on Page 9 P atients with liver cirrhosis and portal hypertension develop renal sodium retention which promotes formation of ascites and peripheral edema. The "underfill theory" initially attributed sodium retention to secondary hyperaldosteronism accounted for by renal hypoperfusion brought about by intraabdominal fluid sequestration. 1 However, the underfill theory cannot explain the early phase of cirrhosis as sodium retention may precedes formation of ascites. 2-7 Thus, the "overflow theory" postulated that edema and ascites formation resulted from primary renal sodium retention promoting plasma volume expansion. 8 This theory is supported by the fact that abolishing portal hypertension in cirrhotic dogs by sideto-side portocaval shunt prevented ascites formation but not sodium retention. 5,6 Later, the "revised underfill theory" proposed that peripheral arterial vasodilatation leading to decreased effec...

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Section: Discussionsupporting

confidence: 78%

mentioning

confidence: 99%

Sodium retention and ascites formation in a cholestatic mice model: Role of aldosterone and mineralocorticoid receptor?

et al. 2007

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“…However, until the activity of ENaC is not measured directly by electrophysiological methods in the renal tubular segments from BDL rats such a mechanism remains speculative. Jonassen et al [18] proposed the thick ascending limb (TAL) and not the CCD to be responsible for abnormal renal sodium retention in BDL rats. They measured Na,K-ATPase activity at V max conditions in microdissected tubules from TAL and outer medullary collecting duct (OMCD) in rats 5 weeks after BDL.…”

Section: Sham Operated Bile Duct Ligationmentioning

confidence: 99%

Sodium retention in rats with liver cirrhosis is associated with increased renal abundance of NaCl cotransporter (NCC)

Yu¹,

Serra²,

Sauter³

et al. 2005

Nephrology Dialysis Transplantation

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“…Chronic bile duct ligation (BDL), a commonly used animal model of obstructive cirrhosis, is associated with elevated circulating AVP, cytokines, and activation of the renin-angiotensin system (33,(37)(38)(39)(40). In this model, TRPV4 protein content is increased in the SON, as is its expression in lipid rafts within the hypothalamus (41).…”

mentioning

confidence: 99%

Region‐Specific Changes in Transient Receptor Potential Vanilloid Channel Expression in the Vasopressin Magnocellular System in Hepatic Cirrhosis‐Induced Hyponatraemia

Nedungadi

Carreño

Walch

et al. 2012

J Neuroendocrinology

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The purpose of this study was to measure the expression of transient receptor potential (TRP) channels in the magnocellular neurons of the paraventricular (PVN) and supraoptic nucleus (SON) in an animal model of hepatic cirrhosis associated with inappropriate vasopressin (AVP) release. In these studies we used chronic bile duct ligation (BDL) in the rat, a commonly used model of hepatic cirrhosis, associated with elevated plasma AVP. This study tested the hypothesis that changes in TRPV channel expression may be related to inappropriate AVP release in BDL rats. To test our hypothesis, we utilized laser capture microdissection of AVP neurons in the PVN and SON and Western blot analysis from brain punches. Laser capture microdissection and qRT-PCR demonstrated elevated TRPV2 mRNA in the PVN and SON of BDL as compared to sham ligated controls. AVP transcription was also increased as determined using intron specific primers to measure heteronuclear RNA. Immunohistochemistry demonstrated increased AVP and TRPV2 positive cells in both the PVN and SON after BDL. Also, there was an increased co-expression of TRPV2 and AVP cells after BDL. However, there was no change in the colocalization counts of TRPV2 and OXY in both the magnocellular regions evaluated. In the SON but not the PVN, transcription levels of TRPV4 was also significantly increased in BDL rats Western Blot analysis of punches containing the PVN and SON revealed that TRPV2 protein content was significantly increased in these brain regions in BDL rats compared to sham. Our data suggests that regionally specific changes in TRPV expression in the MNC AVP neurons could alter their osmosensing ability.

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Collecting duct function in liver cirrhotic rats with early sodium retention

Cited by 6 publications

References 20 publications

Sodium retention and ascites formation in a cholestatic mice model: Role of aldosterone and mineralocorticoid receptor?

Sodium retention and ascites formation in a cholestatic mice model: Role of aldosterone and mineralocorticoid receptor?

Sodium retention in rats with liver cirrhosis is associated with increased renal abundance of NaCl cotransporter (NCC)

Region‐Specific Changes in Transient Receptor Potential Vanilloid Channel Expression in the Vasopressin Magnocellular System in Hepatic Cirrhosis‐Induced Hyponatraemia

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