Role of Aldosterone in Edema Formation

Wolff, H. P.; Bette, L; Blaise, H.; Düsterdieck, G.; Jahnecke, J; Kobayashi, T; Krück, F.; Lommer, D.; Schieffer, Hermann

doi:10.1111/j.1749-6632.1966.tb41203.x

Cited by 48 publications

(14 citation statements)

References 8 publications

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“…These findings during the resting state in chronic experimental low output failure agree with the results on the metabolism of aldosterone in patients with heart failure (3,11,12,17,18) in that MCR was reduced. No data are available on the effect of exercise on aldosterone metabolism in patients with cardiac failure, and the measurements of hepatic blood flow in patients were made (4) on individuals with less heart failure than these experimental animals.…”

Section: Discussionsupporting

confidence: 82%

Metabolism of Aldosterone in Several Experimental Situations with Altered Aldosterone Secretion*

Davis¹,

Olichney²,

Brown³

et al. 1965

J. Clin. Invest.

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In an earlier study (1), the rate of metabolism of aldosterone was found to be decreased in dogs with chronic passive congestion of the liver secondary to thoracic inferior vena caval constriction. After hepatectomy of these animals and of normal dogs, the metabolism of aldosterone was almost abolished. It was suggested that the decreased aldosterone metabolism during liver congestion might be secondary to decreased hepatic blood flow and associated hepatic anoxia. More recently, Tait and his colleagues (2, 3) have provided evidence that the rate of hepatic blood flow is one of the primary determinants of the rate of aldosterone metabolism.The present observations were undertaken to examine the metabolism of aldosterone in several experimental situations in which altered aldosterone secretion occurs and in which there are known or suspected alterations in liver blood flow. The primary objectives were twofold: 1) to define the distribution, metabolic clearance rate (MCR), and hepatic extraction of aldosterone, and 2) to determine the contribution of altered aldosterone metabolism to the peripheral plasma level of aldosterone. Aldosterone metabolism was studied following acute hemorrhage, in dogs depleted of sodium, and in dogs with chronic experimental heart failure. Observations were made in both low and high output failure because hepatic blood flow is reduced in the former and, presumably, normal or elevated in the latter situation. Since exercise greatly reduces the blood flow through the liver in patients with heart failure (4), observations were made before and during ex- hausting exercise in dogs with low output heart failure. The metabolism of aldosterone was also studied in hypophysectomized dogs; in this situation there is a low rather than a high rate of aldosterone secretion, and hepatic blood flow is probably reduced. Finally, the hepatic extraction of aldosterone was measured in several experimental situations. MethodsThe rate of metabolism of aldosterone was studied by observing the rate of disappearance of 1,2-H'-d-aldosterone from peripheral plasma; single iv injections of 12 X 10' cpm of 1,2-H3-d-aldosterone with a SA of 100 Acc per ug were made. The efficiency of the liquid scintillation spectrometer was approximately 25%b. Peripheral venous blood samples of 20 ml were drawn at 5, 10, 15,20, 30, 45, 60, 75, and 90 minutes, and plasma was analyzed for true H3-d-aldosterone. The dogs weighed from 17 to 22 kg.To study the effects of hemorrhage, 30 ml of arterial blood per kg body weight was removed over a 5-to 15-minute period in nine dogs anesthetized with Na pentobarbital. As soon as the arterial pressure had stabilized, tritiated aldosterone was injected, and peripheral venous blood samples were obtained. Arterial pressure was measured continuously throughout the experiment by means of a Statham strain gauge and a Sanborn recording system. As a control experiment, the disappearance of tritiated aldosterone was studied in a series of seven normal dogs anesthetized similarly.Sodium depletion was ...

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Section: Discussionsupporting

confidence: 82%

Metabolism of Aldosterone in Several Experimental Situations with Altered Aldosterone Secretion*

Davis¹,

Olichney²,

Brown³

et al. 1965

J. Clin. Invest.

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“…• Hypersecretion of aldosterone is common in edematous states (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Many patients with congestive heart failure have increased secretion and excretion of aldosterone (1,(3)(4)(5)(6)(7), but patients with edema also have normal rates of secretion, of this hormone (8)(9)(10).…”

Section: Additional Abstractmentioning

confidence: 99%

“…Many patients with congestive heart failure have increased secretion and excretion of aldosterone (1,(3)(4)(5)(6)(7), but patients with edema also have normal rates of secretion, of this hormone (8)(9)(10). Experimental heart failure in dogs is regularly accompanied by an increase in aldosterone…”

Section: Additional Abstractmentioning

confidence: 99%

Plasma Renin in Chronic Experimental Heart Failure and during Renal Sodium "Escape" from Mineralocorticoids

Johnston

Davis

Robb

et al. 1968

Circulation Research

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A striking increase in the plasma renin level occurred in dogs with low output right heart failure secondary to tricuspid insufficiency and pulmonic stenosis and in three of five animals with high output failure produced by a large arteriovenous fistula. When dogs with a small arteriovenous fistula were given daily injections of DOCA, the renal sodium "escape" phenomenon occurred. In these animals, the level of plasma renin was suppressed during DOCA administration both during the initial period of sodium retention and also later when sodium balance was normal or negative. In contrast, when dogs with a larger arteriovenous fistula but without evidence of cardiac failure were given DOCA, they retained sodium and developed signs of congestive heart failure. However, in these animals with congestion and ascites, in contrast to-the dogs that developed spontaneous high output failure, the plasma renin was low. Renin-substrate was unaltered in all of the experimental situations studied except for the decrease observed in dogs with low output right heart failure, la these animals, it seems likely that decreased renin-substrate was secondary to hepatic congestion and liver damage. The renin-angiotensin system does not seem to be related to the "escape" phenomenon, and renin does not appear to be the factor that makes the kidney unusually responsive to mineralocorticoids. Thus, in experimental heart failure the reninangiotensin system was activated, but in the congestive syndrome produced by DOCA the plasma renin level was suppressed. ADDITIONAL KEY WORDSrenin-angiotensin system arteriovenous fistula desoxycorticosterone sodium balance renin-substrate tricuspid insufficiency and pulmonic stenosis high output failure conscious dogs• Hypersecretion of aldosterone is common in edematous states (1-12). Many patients with congestive heart failure have increased secretion and excretion of aldosterone (1, 3-7), but patients with edema also have normal rates of secretion, of this hormone (8-10). Experimental heart failure in dogs is regularly accompanied by an increase in aldosteroneFrom the Departments of Physiology and Surgery, University of Missouri School of Medicine, Columbia, Missouri 6520X.This investigation was supported in part by U. S. Public Health Service Research Grant HE 10612-01 from the National Heart Institute.Dr. Johnston is Research Fellow, National Heart Foundation of Australia.Accepted for publication December 10, 1967. secretion and a high plasma level of aldosterone (2,11,12). The increase in plasma aldosterone in heart failure also results from a decrease in the metabolic clearance of aldosterone by the Ever (4, 9, 13). The present study relates the participation of the reninangiotensin system in experimental heart failure to sodium balance and to the known hypersecfetion of aldosterone. This investigation is also concerned with the role of the renin-angiotensin system in the "escape" phenomenon (14-15). Normal humans or animals given large quantities of a mineralocorticoid retain sodium for only ...

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“…Measure ments of the several components of this system in various clinical conditions, therefore, remain pertinent. One such disease is the nephrotic syndrome in which numerous workers have reported elevated secretion, excretion and plasma concentrations of aldosterone [10,15,17,23,24,26], Several reports indicate variable elevation of both plasma renin activity [1,11,13,18,20,25] and angiotensin [11,16] in nephrotic patients, whereas plasma renin-substrate concentrations are sometimes reduced [1,13], However, so far as we are aware, there are no reports of concurrent estimations of the different com ponents of this system under controlled conditions. These measurements have been made in the studies reported here.…”

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confidence: 99%

A Study of the Renin-Angiotensin System in the Nephrotic Syndrome

Medina¹,

Davies²,

Brown³

et al. 1974

Nephron

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Simultaneous measurements of the plasma concentrations of renin, renin-substrate, angiotensin II and aldosterone were made in seven patients with the nephritic syndrome and in five normal subjects studied under the same controlled conditions. Plasma renin-substrate concentration was found to be reduced in some patients. Although plasma renin concentration was frequently elevated, plasma angiotensin II and aldosterone concentrations were generally within the normal range.

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Role of Aldosterone in Edema Formation

Cited by 48 publications

References 8 publications

Metabolism of Aldosterone in Several Experimental Situations with Altered Aldosterone Secretion*

Metabolism of Aldosterone in Several Experimental Situations with Altered Aldosterone Secretion*

Plasma Renin in Chronic Experimental Heart Failure and during Renal Sodium "Escape" from Mineralocorticoids

A Study of the Renin-Angiotensin System in the Nephrotic Syndrome

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