“…In the present studies it has been shown that after cortisone there is still a clear correlation between filtration rate and sodium output, though the latter is slightly less, and the fraction of filtered sodium reabsorbed slightly higher, than at parallel levels of filtration without cortisone. Thus, though cortisone in- 17 Probably aldosterone (34,35).…”
“…In the present studies it has been shown that after cortisone there is still a clear correlation between filtration rate and sodium output, though the latter is slightly less, and the fraction of filtered sodium reabsorbed slightly higher, than at parallel levels of filtration without cortisone. Thus, though cortisone in- 17 Probably aldosterone (34,35).…”
“…Since its isolation and characterization more than 50 yr ago, 5 investigators have perceived aldosterone primarily as a regulator of extracellular fluid volume and sodium and potassium balance. Aldosterone increases sodium reabsorption in the distal nephron of the kidney by binding to the intracellular mineralocorticoid receptor that translocates to the nucleus, where it upregulates the transcription of genes encoding Na ϩ /K ϩ -ATPase and epithelial sodium channel subunits.…”
“…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).…”
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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