A Simple Radioimmunoassay for Urinary Aldosterone

Langan, John; Jackson, Raul; Adlin, E. Victor; Channick, Bertram J.

doi:10.1210/jcem-38-2-189

Cited by 58 publications

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“…PRA was determined by measuring the production of angiotensin I after incubation of plasma for 2 h at 37 C (26). Urinary cortisol (27) and aldosterone (28) were measured by RIA.…”

Section: Hormone and Other Determinationsmentioning

confidence: 99%

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Adaptation of the Mineralocorticoid Target Tissues to the High Circulating Cortisol and Progesterone Plasma Levels in the Squirrel Monkey^*

et al. 1984

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Many New World primate species have elevated circulating free plasma cortisol concentrations, target tissue resistance to cortisol, and no evidence of sodium retention. A representative New World primate, the squirrel monkey (Saimiri sciureus), has plasma cortisol concentrations above those necessary to cause complete suppression of the renin-angiotensin-aldosterone axis in an Old World primate, the cynomolgus monkey (Macaca fascicularis). Despite this, the arterial blood pressure as well as the plasma sodium, potassium, and bicarbonate levels of the squirrel monkey are similar to those of the cynomolgus monkey, and its plasma aldosterone concentrations are approximately 2-fold higher. These findings suggest that cortisol has minimal sodium-retaining effects in this species. Renal cytosol aldosterone receptor concentrations are about 2- to 3-fold lower in the squirrel monkey than in the cynomolgus, whereas the receptor affinities for [3H]aldosterone are similar in the two monkeys. Higher concentrations of cortisol are needed to displace [3H]aldosterone from the mineralocorticoid receptor in the squirrel monkey than from the renal receptor in the cynomolgus [apparent equilibrium dissociation constant (Ki) = 7.8 X 10(-7) vs. 2.9 X 10(-8) M, respectively]. In addition, in contrast to man and presumably other Old World primates, plasma aldosterone concentrations in the female squirrel monkey do not increase during the reproductive cycle or pregnancy when progesterone concentrations are 10- to 20-fold higher than those of the male or the reproductively quiescent female. This suggests that progesterone is a poor aldosterone antagonist in this species. We conclude that a low concentration of mineralocorticoid receptors in New World Primates is compensated for by higher aldosterone levels, with a concomitant increase in receptor occupancy. The salt-retaining potency of cortisol is low, presumably because of a decrease in the affinity of the aldosterone receptor for glucocorticoids in New World primates.

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“…PRA was determined by measuring the production of angiotensin I after incubation of plasma for 2 h at 37 C (26). Urinary cortisol (27) and aldosterone (28) were measured by RIA.…”

Section: Hormone and Other Determinationsmentioning

confidence: 99%

“…The salt-retaining potency of cortisol is low, presumably because of a decrease in the affinity of the aldosterone receptor for glucocorticoids in New World primates. (Endocrinology 115: [25][26][27][28][29][30][31][32] 1984) …”

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confidence: 99%

Adaptation of the Mineralocorticoid Target Tissues to the High Circulating Cortisol and Progesterone Plasma Levels in the Squirrel Monkey^*

et al. 1984

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“…Renin status was classified by PRA response to sodium depletion with the low sodium protocol. Urinary aldosterone, 23 kallikrein, 18 and prostaglandin determinations were performed on the 24-hour urine samples collected at the end of each of the different dietary sodium periods. Urine samples for kallikrein were stored refrigerated under toluene until the time of assay.…”

Section: Patient Studiesmentioning

confidence: 99%

Urinary excretion of prostaglandin E2, prostaglandin F2 alpha, and thromboxane B2 in normotensive and hypertensive subjects on varying sodium intakes.

et al. 1982

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SUMMARY A deficiency in renal prostaglandins has been implicated in the pathogenesis of essential hypertension, particularly low renin hypertension. Previous studies of urinary prostaglandins as influenced by sodium balance and in essential hypertension have been handicapped by problems with assay methodology, inclusion of male subjects, and/or failure to standardize daily fluid consumption. We compared urinary excretion of prostaglandin E 2 (PGE,), prostaglandin F^ (PGF^), and thromboxane B 2 (TxB 2 ) in black and white normotensive and low-renin and normal-renin hypertensive women during two protocols producing sodium depletion (10 mEq sodium diet) and sodium loading (200 mEq sodium diet plus the fludrohydrocortisone Florinef, a synthetic mineralocorticoid). A constant fluid, potassium, and caloric intake was maintained throughout. Changes in plasma renin activity, urinary aldosterone excretion, and urinary kallikrein excretion were simultaneously assessed.As sodium intake decreased from 120 to 10 mEq sodium/day, increases in urinary PGF^ (502 ± 60 to 1222 ± 176 ng/24 hr, p < 0.01) and TxB ; (99 ± 33 to 216 ± 77 ng/24 hr, p < 0.05) excretion were observed in normotensive subjects. These increases were not observed in the hypertensive patients, possibly because less renin stimulation was achieved during the low sodium diet. Alternatively, subnormal prostaglandin production may have contributed to the lesser renin stimulation. Furthermore, urinary PGF, excretion in hypertensive patients during sodium depletion indicated strong influences of race and renin status; namely, black and normal-renin hypertensives increased urinary PGF^ excretion during sodium depletion whereas white and low-renin hypertensives did not. When white hypertensives and normotensive subjects consumed either 120 or 200 mEq sodium diet, there were no consistent differences in urinary excretion of PGE 2 , PGF^, or TxB 2 . With sodium loading, urinary PGE,, PGF^, and TxB 2 excretion did not change, whereas urinary kallikrein excretion increased. Urinary excretion of these prostanoids was therefore independent of mineralocorticoid and kallikrein effects upon the kidney. Thus, we found no evidence for a role of renal PGE 2 , PGF^, and TxB 2 in natriuresis in humans. Urinary excretion of these prostanoids was decreased in hypertensive patients only during sodium depletion. (Hypertension 4: 735-741, 1982) KEY WORDS • prostaglandins • thromboxane • kallikrein • renin • aldosterone natriuresis • mineralocorticoid escape • sodium loading

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“…Both patients who had levels within the normal range were in Group 3 (presumed bilateral hyperplasia). The mean level of plasma aldosterone in the 35 patients with surgically confirmed adenomas (Group 1) was 2020pmol/L, range 470-4860pmol/L; in the 14 patients in whom there was good evidence of an adenoma but in whom no confirmation was possible the mean level was 13 16 pmol/L, range 600-2925 pmol/L; in the eight patients presumed to have bilateral adrenal hyperplasia (Group 3) the mean level was 1065 pmol/L range 390-4100 pmol/L. None of the four patients on a high salt intake showed suppression of plasma aldosterone to the low levels which other authors have found in normal subjects receiving a high salt Plasma aldosterone responses to change in posture The change in plasma aldosterone level when 30 min mobility followed overnight recumbency was measured in 30 patients on a normal sodium intake.…”

Section: Plasma Aldosteronementioning

confidence: 90%

Primary Hyperaldosteronism in England and Wales: A Review of the Use of a Supraregional Assay Service Laboratory for the Measurement of Aldosterone and Plasma Renin Activity

Short

James

1991

Ann Clin Biochem

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To ascertain the use being made of a Supraregional Assay Service laboratory in the diagnosis of primary hyperaldosteronism, follow-up data were obtained on 60 patients in whom the diagnosis was suggested by the biochemical results. In 36 patients an adrenal adenoma had been removed; 14 patients had evidence of an adenoma on CT scan; 10 patients were presumed to have bilateral adrenal hyperplasia. The data used to make the diagnosis of primary hyperaldosteronism and to assess the likelihood of the presence of an adenoma indicate that patients studied at 40 centres in the UK show results very similar to those of North American series where large numbers of patients have been described but all have been studied in the same centre. The majority of patients in our series were treated at the hospital at which the diagnosis was made, thus avoiding referral to a centre distant from the patient's home and indicating that the service was being used as originally intended when the Supraregional Assay Service was set up.

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A Simple Radioimmunoassay for Urinary Aldosterone

Cited by 58 publications

References 0 publications

Adaptation of the Mineralocorticoid Target Tissues to the High Circulating Cortisol and Progesterone Plasma Levels in the Squirrel Monkey^*

Adaptation of the Mineralocorticoid Target Tissues to the High Circulating Cortisol and Progesterone Plasma Levels in the Squirrel Monkey^*

Urinary excretion of prostaglandin E2, prostaglandin F2 alpha, and thromboxane B2 in normotensive and hypertensive subjects on varying sodium intakes.

Primary Hyperaldosteronism in England and Wales: A Review of the Use of a Supraregional Assay Service Laboratory for the Measurement of Aldosterone and Plasma Renin Activity

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A Simple Radioimmunoassay for Urinary Aldosterone

Cited by 58 publications

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Adaptation of the Mineralocorticoid Target Tissues to the High Circulating Cortisol and Progesterone Plasma Levels in the Squirrel Monkey*

Adaptation of the Mineralocorticoid Target Tissues to the High Circulating Cortisol and Progesterone Plasma Levels in the Squirrel Monkey*

Urinary excretion of prostaglandin E2, prostaglandin F2 alpha, and thromboxane B2 in normotensive and hypertensive subjects on varying sodium intakes.

Primary Hyperaldosteronism in England and Wales: A Review of the Use of a Supraregional Assay Service Laboratory for the Measurement of Aldosterone and Plasma Renin Activity

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Adaptation of the Mineralocorticoid Target Tissues to the High Circulating Cortisol and Progesterone Plasma Levels in the Squirrel Monkey^*

Adaptation of the Mineralocorticoid Target Tissues to the High Circulating Cortisol and Progesterone Plasma Levels in the Squirrel Monkey^*