Isolierung eines neuen kristallisierten Hormons aus Nebennieren mit besonders hoher Wirksamkeit auf den Mineralstoffwechsel

Simpson, Sylvia A.; Tait, John; Wettstein, A.; Neher, R.; Euw, J. v.; Reichstein, T.

doi:10.1007/bf02155834

Cited by 264 publications

(49 citation statements)

References 22 publications

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“…4 Subsequent to the discovery of the potent sodiumretaining hormone, aldosterone, in 1953, 5 it became apparent that increased secretion of this hormone plays an important role in renal sodium conservation during dietary sodium restriction. 6 Under these conditions, the renin-angiotensin system is an important stimulus to aldosterone secretion.…”

Section: Evidence For a Splanchnic Sodium Input Monitor Regulating Rementioning

confidence: 99%

Evidence for a splanchnic sodium input monitor regulating renal sodium excretion in man. Lack of dependence upon aldosterone.

Carey¹

1978

Circulation Research

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SUMMARY Eight normal male subjects were placed on a constant 10 mEq sodium, 60 mEq potassium diet for 5 days. At 8:00 a.m. on the 5th day, the subjects were given a standard dose of 100 mEq of sodium orally or intravenously. Subjects receiving oral sodium also received 200 ml of 5% dextrose in water intravenously, and those receiving intravenous sodium also received placebo capsules orally. Water intake and posture were controlled. The subjects then returned to a free diet for 1 month and subsequently were restudied by using the opposite route of sodium administration. The subjects given the oral sodium load excreted greater quantities of sodium in their urine than those repleted intravenously. The differential natriuresis was significant as early as 2 hours after sodium loading. Plasma aldosterone concentration was similar irrespective of the route of sodium administration. Six patients with primary adrenocortical insufficiency and documented hypoaldosteronism were studied with the same protocol after 5 days of 50 mEq sodium, 60 mEq potassium intake. They also had significantly greater natriuresis after oral than intravenous sodium administration. The data suggest the presence of a splanchnic input monitor for sodium which partially regulates renal sodium excretion and is not dependent upon a turn-off mechanism for aldosterone secretion.DIETARY sodium depletion in man is followed by rapid conservation of sodium by the kidneys.

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Section: Evidence For a Splanchnic Sodium Input Monitor Regulating Rementioning

confidence: 99%

Evidence for a splanchnic sodium input monitor regulating renal sodium excretion in man. Lack of dependence upon aldosterone.

Carey¹

1978

Circulation Research

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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: 96%

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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“…1 Sodium transport, and hence salt balance, is regulated by a number of mechanisms; however, aldosterone has a critical role. Aldosterone exerts its effects on the distal nephron (and colon) as the last point of sodium reabsorption; it is thus the final arbiter.…”

mentioning

confidence: 99%

Mechanisms of Mineralocorticoid Action

Fuller¹,

Young²

2005

Hypertension

275

169

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Abstract-Sodium transport in epithelial tissues is regulated by the physiological mineralocorticoid aldosterone. The response to aldosterone is mediated by the mineralocorticoid receptor (MR), for which the crystal structure of the ligand-binding domain has recently been established. The classical mode of action for this receptor involves the regulation of gene transcription. Several genes have now been shown to be regulated by aldosterone in epithelial tissues. Of these, the best characterized is serum-and glucocorticoid-regulated kinase, which increases sodium influx through the epithelial sodium channel. Turnover of these channels in the cell membrane is mediated by Nedd4 -2, a ubiquitin protein ligase; serum-and glucocorticoid-regulated kinase interacts with and phosphorylates Nedd4 -2, thereby rendering it unable to bind the sodium channels. Key Words: aldosterone Ⅲ sodium channels Ⅲ fibrosis T he isolation of aldosterone just over 50 years ago established it as the primary physiological mineralocorticoid. 1 Sodium transport, and hence salt balance, is regulated by a number of mechanisms; however, aldosterone has a critical role. Aldosterone exerts its effects on the distal nephron (and colon) as the last point of sodium reabsorption; it is thus the final arbiter. 2,3 The importance of aldosterone in the maintenance of sodium homeostasis is seen in a series of monogenetic causes of hypertension, 2 in Conn's syndrome, and in disorders in which mineralocorticoid action is compromised with consequent, life-threatening salt losses. 3 Although other pathophysiological consequences of aldosterone excess were identified by Selye 4 over 60 years ago, their significance has only recently been appreciated. Evidence from the Randomized ALdactone Evaluation Study (RALES) and EPlerenone neuroHormonal Efficacy and SUrvival Study (EPHESUS) trials of beneficial effects of mineralocorticoid antagonist therapy on morbidity and mortality in cardiac failure has focused attention beyond the kidney to effects of mineralocorticoids more broadly in the cardiovascular system. 5 Although an understanding of the molecular basis of aldosterone action has tended to lag behind advances in the biology of other steroid hormones, the last decade has seen significant advances toward an understanding of the mechanisms of mineralocorticoid action. The primary mediator of the response to aldosterone is the mineralocorticoid receptor (MR), the ligand-binding domain (LBD) of which has been recently crystallized. 6 -8 Although the MR primarily acts as a transcription factor, recent evidence suggests that it may also mediate nongenomic (or nonnuclear) activation of second messenger pathways. In addition, there is a growing body of evidence that some actions of aldosterone may involve a receptor other than the MR. The cellular and molecular mediators, including proteins induced by aldosterone, have been characterized in sodium transporting epithelia; however, the critical molecular events in the vasculature remain to be determined. In this brief r...

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Isolierung eines neuen kristallisierten Hormons aus Nebennieren mit besonders hoher Wirksamkeit auf den Mineralstoffwechsel

Cited by 264 publications

References 22 publications

Evidence for a splanchnic sodium input monitor regulating renal sodium excretion in man. Lack of dependence upon aldosterone.

Evidence for a splanchnic sodium input monitor regulating renal sodium excretion in man. Lack of dependence upon aldosterone.

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

Mechanisms of Mineralocorticoid Action

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