Excretion of sodium-retaining substances in patients with congestive heart failure

Singer, Bertha; Wener, J.

doi:10.1016/0002-8703(53)90127-6

Cited by 64 publications

(13 citation statements)

References 18 publications

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“…Studies (1)(2)(3)(4)(5) of patients with congestive heart failure, decompensated hepatic cirrhosis and nephrosis have provided evidence of increased amounts of aldosterone or aldosterone-like substances in urine during edema or ascites formation. More recently, it has been demonstrated (6) that increased urinary excretion of aldosterone occurs in association with sodium retention in dogs with right heart failure and in dogs with ascites secondary to constriction of the thoracic inferior vena cava.…”

mentioning

confidence: 99%

Increased Aldosterone Secretion in Dogs With Right-Sided Congestive Heart Failure and in Dogs With Thoracic Inferior Vena Cava Constriction

Davis¹,

Pechet²,

Ball³

et al. 1957

J. Clin. Invest.

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Studies (1-5) of patients with congestive heart failure, decompensated hepatic cirrhosis and nephrosis have provided evidence of increased amounts of aldosterone or aldosterone-like substances in urine during edema or ascites formation. More recently, it has been demonstrated (6) that increased urinary excretion of aldosterone occurs in association with sodium retention in dogs with right heart failure and in dogs with ascites secondary to constriction of the thoracic inferior vena cava. The data in both man and dog imply that the blood level of aldosterone is elevated.Numerous attempts have been made to elucidate the mechanism regulating aldosterone secretion in clinical states associated with the formation of edema, but no data have been reported to show that increased circulating aldosterone results from increased secretion rather than from a decreased rate of inactivation. The purpose of this study was to determine the relative rates of secretion of aldosterone in 1) dogs with cardiac failure produced by stenosis of the pulmonary artery, 2) dogs with thoracic inferior vena cava constriction and ascites, and 3) normal dogs. METHODSRight heart failure was produced in four dogs by controlled progressive constriction of the main pulmonary artery by a method described previously (7). In three other animals, ascites formed following constriction of the thoracic inferior vena cava. Six normal dogs provided the control material. All animals were female mongrel dogs weighing 15 to 23 kg. The dogs were fed a synthetic diet containing 60 mEq. of sodium and 18 mEq. of potassium per day with two exceptions; one dog with heart failure and one normal dog received 40 mEq. The procedure for isolation of aldosterone from adrenal venous and peripheral blood is shown in Figure 1. An aqueous acetone extract of the blood was concentrated by evaporation in an atmosphere of nitrogen and partitioned twice between petroleum ether and aqueous 70 per cent ethanol. The aqueous ethanol extract was similarly concentrated and then extracted with methylene chloride. This methylene chloride extract was concentrated and 689

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confidence: 99%

Increased Aldosterone Secretion in Dogs With Right-Sided Congestive Heart Failure and in Dogs With Thoracic Inferior Vena Cava Constriction

Davis¹,

Pechet²,

Ball³

et al. 1957

J. Clin. Invest.

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“…That aldosterone is involved in the formation of edema is indicated by an increased urinary output of this hormone by patients with edema caused by heart failure, portal cirrhosis or nephrosis (8)(9)(10)(11)(12)(13).…”

mentioning

confidence: 99%

The Effect of Changes in Body Sodium on Extracellular Fluid Volume and Aldosterone and Sodium Excretion by Normal and Edematous Men 1

Duncan¹,

Liddle²,

Bartter³

et al. 1956

J. Clin. Invest.

117

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The presence of a sodium-retaining hormone, aldosterone, in the adrenal gland and adrenal venous blood (1-4), the increased urinary excretion of aldosterone during sodium depletion (5, 6) and the inability of men and animals with adrenal insufficiency to conserve sodium support the concept that the process by which the sodium content and thus the extracellular fluid (ECF) volume of the body are regulated includes adrenocortical control of sodium excretion by aldosterone secretion (7).That aldosterone is involved in the formation of edema is indicated by an increased urinary output of this hormone by patients with edema caused by heart failure, portal cirrhosis or nephrosis (8-13).The present work further defines the role of aldosterone in the control of ECF volume of normal men and in the formation of edema by patients with heart failure or portal cirrhosis. METHODSThe patients lived on a metabolic ward during the studies. Constant diets were prepared from uniform lots of food. The patients were weighed each morning after voiding and before breakfast. Blood samples were drawn 3 times a week before breakfast. Total collections of urine and feces were made. Urine was kept at 5°C. during and following collection. Sodium and potassium in diets, urine, feces and sera, and cation exchange resin in feces were determined as previously described (14 (Circulation, 1955, 12, 697).Sodium uptake is thus the percentage of the total exchange capacity of the resin occupied by sodium. The uptake of potassium by resin was calculated in the same fashion on the assumption that there were 10 mEq. of potassium per day uncombined with resin in the stool. The results are essentially the same if it is assumed that all of the sodium and potassium in the stool is combined with resin.

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“…Over the past five years there has accumulated convincing evidence that the clinical conditions which are characterized by pathological accumulation of sodium (e.g., congestive heart failure, cirrhosis with ascites, and nephrosis) are also characterized by high urinary levels of sodiumretaining steroids (9)(10)(11)(12). High levels of these steroids have also been found in the urine of healthy subjects in whom the stimulus to sodium conservation has been provided by a low-sodium diet (10).…”

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confidence: 99%

The Physiological Basis for a Method of Assaying Aldosterone in Extracts of Human Urine

Liddle¹,

Cornfield²,

Casper³

et al. 1955

J. Clin. Invest.

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Excretion of sodium-retaining substances in patients with congestive heart failure

Cited by 64 publications

References 18 publications

Increased Aldosterone Secretion in Dogs With Right-Sided Congestive Heart Failure and in Dogs With Thoracic Inferior Vena Cava Constriction

Increased Aldosterone Secretion in Dogs With Right-Sided Congestive Heart Failure and in Dogs With Thoracic Inferior Vena Cava Constriction

The Effect of Changes in Body Sodium on Extracellular Fluid Volume and Aldosterone and Sodium Excretion by Normal and Edematous Men 1

The Physiological Basis for a Method of Assaying Aldosterone in Extracts of Human Urine

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