The Regulation of Aldosterone Secretion in Man: The Role of Fluid Volume 1

Bartter, Frederic C.; Liddle, Grant W.; Duncan, Leroy E.; Barber, Joan K.; Delea, Catherine S.

doi:10.1172/jci103386

Cited by 233 publications

(50 citation statements)

References 15 publications

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“…However, water loading can lead to depressed proximal tubular reabsorption ofsodium, by intrarenal mechanisms (Martino & Earley, 1967). Furthermore, expansion of extracellular fluid and plasma volumes would cause reduced aldosterone production (Bartter, Liddle, Duncan, Barber & Delea, 1956) and, therefore, reduced tubular reabsorption of sodium.…”

Section: Discussionmentioning

confidence: 99%

Effects of water diuresis and osmotic (mannitol) diuresis on urinary solute excretion by the conscious rat

Atherton¹,

Hai²,

Thomas³

1968

The Journal of Physiology

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SUMMARY1. The time course and extent of changes in urinary flow and in the outputs of urea, Na+, K+, and NH+ over a period of 71 hr in conscious rats during water and osmotic (mannitol) diuresis were determined, and compared with spontaneous changes in non-diuretic animals.2. In non-diuretic rats, a morning rise and subsequent decline in urinary osmolal, sodium, potassium and ammonium outputs occurred, possibly attributable to circadian rhythms.3. Water diuresis was accompanied by (i) a rapid increase in urea excretion during the phase of increasing urine flow, followed by a fall in later periods to values similar to those in non-diuresis, (ii) a slower increase in sodium output, continuing after the establishment of the constant water load, (iii) unchanged potassium excretion, but slightly increased ammonium outputs.

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Section: Discussionmentioning

confidence: 99%

Effects of water diuresis and osmotic (mannitol) diuresis on urinary solute excretion by the conscious rat

Atherton¹,

Hai²,

Thomas³

1968

The Journal of Physiology

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“…2 It has previously been suggested that aldosterone secretion is regulated by some function of extracellular (8) Farrell (10) has suggested that aldosterone secretion is regulated principally by means of intracranial receptors, primarily measuring sodium concentration. Evidence from experiments in man, on the other hand, suggests that neither serum sodium concentration nor total body sodium can control aldosterone secretion, which can be made to vary independently of both (8). The (9).…”

Section: Discussionmentioning

confidence: 99%

Increase in Aldosterone Secretion by Carotid Artery Constriction in the Dog and Its Prevention by Thyrocarotid Arterial Junction Denervation *

Bartter¹,

Mills²,

Gann³

1960

J. Clin. Invest.

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Although it has been shown that the vagus nerves may carry impulses mediating decreases in the rate of aldosterone secretion (1), no equivalent pathway has been demonstrated which might mediate increases in aldosterone secretion. Because of evidence that aldosterone secretion may be increased by some function of a decreased intravascular volume (2), and the evidence cited above that this increase is not dependent upon the integrity of intrathoracic vagal receptors (1), the present experiments were designed to investigate the role of receptors located in the arterial system. METHODSAcute experiments were performed on mongrel dogs under pentobarbital anesthesia. The lumboadrenal veins were cannulated (3) and blood samples were collected intermittently for determination of aldosterone by Mills, Casper and Bartter's modification (1) of the method of Neher and Wettstein (4). This method has an absolute sensitivity of 0.1 ,ug of aldosterone. Losses during extraction and chromatography were determined on every sample by adding C,4-cortisone to each specimen before extraction and counting the cortisone region on the final chromatogram after development of the soda fluorescence. The mean recovery rate was 42 ± 9 per cent (SD). The overall sensitivity, considering the amount of the sample taken for analysis and the recovery rate, was 0.5 ,ug per hour. The final value was corrected for all losses by dividing each observed value by the rate of recovery of that sample. Thus, the only variable altering reproducibility is that of measurement of the soda fluorescence on paper. The technique used was that described by Ayres, Simpson and Tait (5) who found that, in measuring 0.5 Ag of aldosterone diacetate, the standard error was 0.01 and the standard errors for measurement of 2, 4, and 8 ,ug were, respectively, 0.17, 0.43, and 0.73. In experiments in this laboratory, the standard error for measurement of 1 ,ug of cortisone was found to be 0.04. Aldosterone secretion was stimulated by supradiaphragmatic inferior vena cava constriction (6) in 29 experiments. In 22 studies the stimulus was bilateral con-

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“…It lhas been demonstrated that administration of sodium to normal individuals either by increasing dietary sodium intake or by giving an intravenous load of saline decreases aldosterone secretion or excretion (1)(2)(3)(4)(5)(6). The relationship between the response of the renin-angiotensin system and aldosterone to a sodium load has been less clearly defined.…”

Section: Introductionmentioning

confidence: 99%

Studies of the Control of Plasma Aldosterone Concentration in Normal Man

Williams¹,

Tuck²,

Rose³

et al. 1972

J. Clin. Invest.

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A B S T R A C T The peripheral plasmna levels of aldosterone, renin activity, potassium, sodium, corticosterone, and cortisol were measured in six normal subjects four times daily-10 a.m., 2 p.m., 5 p.m., 11 p.m.-on 3 consecutive days. A constant daytime activity program was maintained throughout the study. After 5 days on a 10 mEq sodium/100 mEq potassium isocaloric intake, the mean upright 10 a.m. plasma renin activity was 1773±186 ng/100 xnl per 3 hr and the mean plasma aldosterone, 81±+14 ng/100 ml. These two parameters fell continuously throughout the day parallel to the fall in plasma cortisol and corticosterone. In response to 2 liters of normal saline infused from 10 a.m. to 2 p.m. on 2 consecutive days, plasma aldosterone levels fell significantly to 13±5 ng/100 ml at 2 p.m. after the 1st day's infusion and to 6±1 ng/100 ml at 2 p.m. after the 2nd. Plasma renin activity demonstrated a parallel fall to 368±63 ng/ 100 ml per 3 hr and 189±27 ng/100 ml per 3 hr at 2 p.m. on the 1st and 2nd days, respectively. There was no significant alteration in plasma levels of cortisol, corticosterone, potassium, or sodium on the 2 days of sodium loading in comparison with the control day. In an additional study, five normal supine subjects received 500 ml saline/hr for 6 hr. As in the 2 day study, plasma aldosterone and renin activity had parallel decrements at 1, 2, 4, and 6 hr after the start of the saline infusion. From these studies, it is concluded that plasma renin activity is the dominant factor controlling plasma aldosterone when sodium-depleted normal subjects are acutely repleted.Dr. Williams is an Investigator of the Howard Hughes Medical Institute.

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The Regulation of Aldosterone Secretion in Man: The Role of Fluid Volume 1

Cited by 233 publications

References 15 publications

Effects of water diuresis and osmotic (mannitol) diuresis on urinary solute excretion by the conscious rat

Effects of water diuresis and osmotic (mannitol) diuresis on urinary solute excretion by the conscious rat

Increase in Aldosterone Secretion by Carotid Artery Constriction in the Dog and Its Prevention by Thyrocarotid Arterial Junction Denervation *

Studies of the Control of Plasma Aldosterone Concentration in Normal Man

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