A Study of the Mechanism of Secretion of the Sodium-Retaining Hormone (Aldosterone)12

There is extensive evidence that provision of potassium as well as sodium may be of vital importance in the treatment of a wide variety of metabolically disturbed patients (1-3). Physicians sometimes are hesitant to administer potassium, however, because they are concerned that such therapy may result in potassium intoxication.The present studies were undertaken in an effort to gather information which would facilitate considerations of this problem.Specifically, the aims of this study were threefold: The first was to determine the upper limit of potassium intake compatible with body potassium homeostasis.

Section: Observationsmentioning

confidence: 99%

A Study of the Effects of Excessive Potassium Intake upon Body Potassium Stores1

Drescher¹,

Talbot²,

Meara³

et al. 1958

“…Previous studies have shown that aldosterone production can be markedly influenced by changes in potassium ( [1][2][3][4][5]. It is still uncertain, however, whether the modulating effect of potassium is dependent upon gross changes in potassium balance or whether it may also occur in response to changes in plasma potassium concentration independently of changes in potassium balance.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Plasma Aldosterone Concentration by Plasma Potassium in Anephric Man in the Absence of a Change in Potassium Balance

Cooke¹,

Horvath²,

Moore³

et al. 1973

A B S T R A C T In studies on seven anephric patients, glucose and insulin administration before hemodialysis produced a significant reduction in plasma potassium concentration (mean reduction = 1.3, 1.7, and 1.4 meq/ liter at 60, 120, and 180 min, respectively) which was accompanied by a significant and sustained reduction in plasma aldosterone concentration. There was a significant correlation between plasma aldosterone and plasma potassium concentration (r = +0.74, P < 0.001) and between changes in the concentration of plasma aldosterone occurring in individual patients and the corresponding changes in plasma potassium concentration (r = +0.52, P < 0.01). There was no significant change in plasma sodium concentration, and plasma corticoid concentration, which was monitored as an index of ACTH elaboration, was reduced at 60 min but increased subsequently as symptoms attributable to hypoglycemia were observed.These studies demonstrate that plasma aldosterone concentration can be modulated acutely by transitory changes in plasma potassium concentration without a change in potassium balance. The effect of glucose and insulin administration on intracellular potassium in the adrenal cortex is uncertain, and although increased net movement of potassium into cells is the presumptive mechanism of the reduction in plasma potassium concen-

“…In man, on low or normal sodium intakes, potassium loading has been associated with increased urinary excretion or secretion of aldosterone (3)(4)(5)(6)(7). In man, however, acute changes in aldosterone secretion in response to small changes in serum potassium have not been documented.…”

Section: Introductionmentioning

confidence: 99%

Studies of the control of plasma aldosterone concentration in normal man

Dluhy¹,

Axelrod²,

Underwood³

et al. 1972

158

A B S T R A C T The responses of plasma aldosterone, cortisol, and corticosterone to an infusion of 75 mEq of potassium chloride over 120 min were studied in 10 normal subjects. Five subjects were fed a 10 mEq and five a 200 mEq sodium diet, while all subjects ingested 40 mEq and 200 mEq potassium sequentially. Two potassium infusions were performed in each subject when in balance on a fixed sodium intake and low and then high potassium diets.Regardless of dietary intake, increases of serum potassium of 0.5-1.5 mEq/liter above preinfusion levels were usually associated with significant increments in plasma aldosterone concentration. Our data agree with previous evidence that the potassium ion stimulates the adrenal cortex directly to secrete aldosterone. Peripheral renin activity did not increase after the potassium infusion. Plasma cortisol and corticosterone levels generally followed the expected diurnal decline during the infusion, implying that ACTH secretion did not in-