The Effect of Adrenal Extract on Mineral Metabolism

Tait, John; Simpson, Sylvia A.; Grundy, H. M.

doi:10.1016/s0140-6736(52)92427-6

Cited by 86 publications

(25 citation statements)

References 5 publications

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“…In 1952 Tait et al [85] reported the sodiumretaining effect of an unidentified adrenal extract; and in 1953 Simpson et al [78] described the crystallization of this sub stance. Initially named sodium-retaining corticoid by Luetscher and co-workers [54,56] and electrocortin by Simpson et al [77], this hormone was renamed aldosterone when its structure was determined in 1954 [79].…”

Section: Early Studies: 1950-1956mentioning

confidence: 99%

Aldosterone and Renal Potassium Excretion

Rabinowitz¹

1979

Kidney Blood Press Res

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Section: Early Studies: 1950-1956mentioning

confidence: 99%

Aldosterone and Renal Potassium Excretion

Rabinowitz¹

1979

Kidney Blood Press Res

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“…The presence of a sodium-retaining hormone, aldosterone, in the adrenal gland and adrenal venous blood (1)(2)(3)(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).…”

mentioning

confidence: 97%

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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“…This steroid has been isolated from adrenal tissue (3)(4)(5), from adrenal venous blood of animals (6, 7) and from human urine (8,9).…”

mentioning

confidence: 99%