The role of renin and aldosterone in the salt retention of edema

Chonko, Arnold M.; Bay, William H.; Stein, Janice Gross; Ferris, Thomas F.

doi:10.1016/0002-9343(77)90541-1

Cited by 115 publications

(37 citation statements)

References 19 publications

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“…In the sodium-repleted state, 2 (43) supports this hypothesis. In a group of patients with massive peripheral edema, the normal hemodynamic response to head up was blunted.…”

Section: Discussionmentioning

confidence: 54%

“…For instance, Ayers and coworkers have shown that sodium retention can be virtually complete, despite a relatively normal aldosterone secretory rate (1). Chonko and co-workers identified two responses to sodium loading in heart failure (2). One was associated with persistent activation of the renin angiotensin system, while the second group retained sodium despite suppression of the renin angiotensin system.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Sodium and water balance in chronic congestive heart failure.

Cody¹,

Covit²,

Schaer³

et al. 1986

J. Clin. Invest.

163

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As the characteristics of sodium and water balance in heart failure remain undefined, we evaluated the hemodynamic, metabolic, and hormonal effects of balanced sodium intake in 10 patients with chronic congestive heart failure. We discontinued diuretics to avoid their confounding influence, and all patients received 1 wk of 10 meq and 100 meq balanced sodium intake and controlled free water. Comparing sodium intake of 10 with 100 meq, the following observations were made. There was weight gain (2.0 kg) and increased sodium excretion (11±3 to 63±15 meq/24 h), unaccompanied by increase of blood volume. Both renin-angiotensin system and sympathetic nervous system activity were greater during the 10 meq diet, and suppressed with the 100 meq sodium diet. For both diets, plasma renin and urinary aldosterone excretion were correlated with urnary sodium excretion (r = -0.768, r = -0.726, respectively; P < 0.005). Systemic hemodynamics were minimally changed with increased sodium intake. However, reversal of vasoconstriction by captopril during the 10 meq diet, and its ineffectiveness during the 100 meq diet, indicated a renin-dependent mechanism in the former, and a renin-independent mechanism in the latter diet. There were two subgroups of response to the 100 meq diet: one group (a = 5) achieved neutral balance, while the second (a = 5) avidly retained sodium and water. Renin-angiotensin system activity was significantly higher in the latter group, and the mechanism for differences in sodium excretion for the subgroups could not be identified by blood volume or hemodynamic parameters. Orthostatic hypotension during tilt was greater during the 10 meq sodium diet, and in all cases, related to ineffective hemodynamic and hormonal compensatory responses.

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“…In the sodium-repleted state, 2 (43) supports this hypothesis. In a group of patients with massive peripheral edema, the normal hemodynamic response to head up was blunted.…”

Section: Discussionmentioning

confidence: 54%

Section: Introductionmentioning

confidence: 99%

Sodium and water balance in chronic congestive heart failure.

Cody¹,

Covit²,

Schaer³

et al. 1986

J. Clin. Invest.

163

View full text Add to dashboard Cite

show abstract

“…According to this theory, the sodium retention occurs in a manner identical to that resulting from any other hypovolemic stimulus, and is characterized in part by increases in filtration fraction and renal vascular resistance, enhanced fractional reabsorption offiltrate in the proximal tubule, heightened sympathetic renal nerve activity, activation of the renin-angiotensin system, and a reduced concentration of atrial natriuretic peptide (ANP)' in plasma. Numerous clinical and experimental observations document these patterns ofrenal function in at least some forms of nephrotic syndrome and thereby support the so-called "underfill" mechanism of edema formation (2)(3)(4)(5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 81%

Cellular basis for blunted volume expansion natriuresis in experimental nephrotic syndrome.

Valentin¹,

Qiu²,

Muldowney³

et al. 1992

J. Clin. Invest.

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“…2,4,7,[19][20][21][22] Furthermore, saline loading decreased plasma renin and aldosterone in patients with cirrhosis without resolving sodium retention. 23 To reconcile these findings, it has been proposed that aldosterone sensitivity was increased in cirrhosis. [24][25][26][27] This apparent high sensitivity to aldosterone might be accounted for in fact by the abnormal activation of MR by glucocorticoids.…”

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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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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The role of renin and aldosterone in the salt retention of edema

Cited by 115 publications

References 19 publications

Sodium and water balance in chronic congestive heart failure.

Sodium and water balance in chronic congestive heart failure.

Cellular basis for blunted volume expansion natriuresis in experimental nephrotic syndrome.

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

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