Reciprocal Variations in Urinary Cortisol and Aldosterone in Response to Increased Salt Intake in Humans

Ehrlich, Edward N.; Lugibihl, Kathleen; Laves, M.; Janulis, Mark

doi:10.1210/jcem-26-10-1160

Cited by 27 publications

(15 citation statements)

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“…Salt loading has been demonstrated to increase urinary free cortisol excretion in healthy subjects [7][8][9]. In the present study, the changes in urinary free cortisol excretion were not significant in either group.…”

Section: Figurecontrasting

confidence: 66%

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Decreased cortisol production in male type 1 diabetic patients

Kerstens

Luik

Kleij

et al. 2003

Eur J Clin Investigation

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The sum of urinary cortisol metabolite excretion as a measure of cortisol production is lower in nonobese, normotensive type 1 diabetic males with adequate glycaemic control and without severe complications, irrespective of sodium intake. We suggest that this is at least in part as result of diminished 5alpha reductase activity, resulting in a decreased cortisol metabolic clearance. In type 1 diabetic and in healthy males, the 11betaHSD setpoint is not affected by physiological variations in sodium intake.

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Section: Figurecontrasting

confidence: 66%

“…However, the subjects in these studies were heterogeneous with respect to relevant variables such as obesity and gender, which might have confounded the results [6]. Moreover, despite the fact that a high sodium intake may increase urinary free cortisol excretion, none of these studies was controlled for dietary sodium [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Decreased cortisol production in male type 1 diabetic patients

Kerstens

Luik

Kleij

et al. 2003

Eur J Clin Investigation

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“…20 However, extraordinary concentration of PGE have been found in the uterine vein of pregnant rabbits. 8 Whether uterine PGE secretion would increase plasma PGE concentration depends upon the extent to which PGE escapes metabolism during transit through the pulmonary circulation. Studies in the cat and dog 21 indicate that 90-95% of PGEj is metabolized in one passage through the pulmonary capillary bed but in humans only 65% of PGE?…”

Section: Resultsmentioning

confidence: 99%

Factors controlling plasma renin and aldosterone during pregnancy.

Bay¹,

Ferris²

1979

Hypertension

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SUMMARYThe response of plasma renin activity (PR A) and plasma aldosterone (PA) to change in sodium intake was evaluated in pregnant women during the third trimester. After 7 days on a 10 mEq sodium diet, PRA rose from 20.6 ± 6.2 to 59.6 ± 11.6 ng/ml/hr and PA from 47 ± 11 to 127 ± 27 ng% in pregnant women compared to PRA from S ± 1.2 to 18.9 ± 5.2 ng/ml/hr and PA from 7.7 ± 1 to 42 ± 3 ng% in nonpregnant controls. Pregnant women conserved sodium normally with urinary sodium excretion and weight loss similar to nonpregnant women. After 6 days on a 300 mEq sodium intake, PRA and PA in pregnant women were significantly higher, 10.2 ± 1.4 ng/ml/hr and 22 ± 3 ng%, respectively, compared to 1.5 ± 0J ng/ml/hr and 7.3 ± 1 ng% in controls. On both low-and high sodium intake there was a positive correlation between PRA and PA in pregnant women. Plasma prostaglandin E (PGE) was 0.45 ± 0.06 ng/ml in pregnant women compared to 0.1 ± 0.01 ng/ml in control women (p < 0.01) and urinary PGE excretion was 2780 ± 357 ng/24 hr in 28 pregnant women compared to 1191 ± 142 ng/24 hrs (p < 0.01) in 14 nonpregnant controls. These findings indicate that although renin and aldosterone secretion respond to change in sodium intake in pregnancy, the cause of the increased renin secretion of pregnancy may be secondary to the increase that occurs in prostaglandin synthesis. This has been attributed to either a salt-losing tendency induced by the increase in glomerular filtration rate (GFR) and progesterone secretion, 1 -2 orthostatic pooling in the extremities, or increased shunting of blood in the uterine circulation. However, blood volume, cardiac output, renal blood flow, and GFR all increase in pregnancy, which argues against functional volume depletion. In addition, the rise in renin secretion occurs in the first trimester before a great increase in uterine size or blood flow. Some studies 1 ' '• * have suggested no correlation between plasma renin activity (PRA) and plasma aldosterone 410(PA) in pregnancy, which suggests that factors other than sodium balance control renin secretion in pregnancy. To evaluate these questions, studies of PRA and PA were carried out in pregnant women in their third trimester on a low-and high-sodium intake. Since decreased sensitivity to angiotensin occurs during human pregnancy and renal prostaglandin synthesis may affect renin secretion, plasma and urinary PGE were also measured. MethodsNormotensive women in their third trimester with no past history of renal or cardiovascular disease were admitted to the Clinical Research Center and placed on either a 10 or 300 mEq sodium, 100 mEq potassium diet. Plasma renin and aldosterone were obtained before arising and at noon. Daily plasma electrolytes and 24-hour urine samples were obtained for creatinine clearance, urinary sodium and potassium determination. Nonpregnant hospital employees served as controls and were placed on the same diets, but were allowed to leave the metabolic unit during working hours. Plasma renin activity was measured by radioimmunoassay ...

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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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Reciprocal Variations in Urinary Cortisol and Aldosterone in Response to Increased Salt Intake in Humans

Cited by 27 publications

References 1 publication

Decreased cortisol production in male type 1 diabetic patients

Decreased cortisol production in male type 1 diabetic patients

Factors controlling plasma renin and aldosterone during pregnancy.

Studies of the Control of Plasma Aldosterone Concentration in Normal Man

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