A Comparison of Double-Isotope Derivative and Radioimmunological Estimation of Plasma Aldosterone Concentration in Man

Fraser, Robert; Guest, Sheena; Young, J.

doi:10.1042/cs0450411

Cited by 76 publications

(41 citation statements)

References 5 publications

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“…Intra-assay coefficient of variation was 10%, interassay 12%. Plasma aldosterone concentrations (PA) were determined by radioimmunoassay (Fraser et al, 1973). Urine kallikrein activity (UKA) was measured by the method of Amunsden et al (1979) in which the enzyme degrades a chromogenic substrate.…”

Section: Methodsmentioning

confidence: 99%

(+)‐sulpiride antagonises the renal effects of gamma‐L‐glutamyl‐L‐dopa in man.

MacDonald

Jeffrey

Freestone

et al. 1988

Brit J Clinical Pharma

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The Royal Infirmary, Edinburgh EH3 9YW 1 y-L-glutamyl-L-dopa (gludopa) was given by intravenous infusion to six healthy saltreplete men on two occasions, with and without pretreatment with (+)-sulpiride. 2 Gludopa increased sodium excretion, glomerular filtration rate and effective renal plasma flow whilst decreasing plasma renin activity. 3 (+)-sulpiride had no significant effect on baseline natriuresis, renal haemodynamics or plasma renin activity, but significantly attenuated the rise in sodium excretion, glomerular filtration rate and effective renal plasma flow produced by gludopa. 4 (+)-sulpiride abolished the acute fall in plasma renin activity seen with gludopa. 5 (+)-sulpiride raised serum prolactin concentration but did not affect the rise in urine dopamine excretion rate caused by gludopa. 6 Gludopa exerts its renal effects by stimulating specific dopamine receptors which are principally of the DA1 subtype.

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Section: Methodsmentioning

confidence: 99%

(+)‐sulpiride antagonises the renal effects of gamma‐L‐glutamyl‐L‐dopa in man.

MacDonald

Jeffrey

Freestone

et al. 1988

Brit J Clinical Pharma

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“…On days 1 and 8 at times 0 and again 6 h and 24 h after drug administration, measurements were made of plasma active renin concentration (normal range 10-50 mu/l) (Millar et al, 1978), blood angiotensin I (normal range 3-15 pmol/l) (Waite, 1973), plasma angiotensin II (normal range 5-35 pmol/l) (Atkinson et al, 1980), plasma aldosterone (normal range < 500 pmol/l) (Fraser et al, 1973), plasma cortisol (normal range 140-700 nmol/l) and serum converting enzyme activity (ACE) (Cushman & Cheung, 1971;Anderson et al, 1981). As (Miller, 1966 Supine heart rate did not change with treatment and there were similar rises of pulse rate with both compounds and with placebo on standing.…”

Section: Introduction Methodsmentioning

confidence: 99%

Enalapril (MK421) and its lysine analogue (MK521): a comparison of acute and chronic effects on blood pressure, renin‐angiotensin system and sodium excretion in normal man.

Hodsman¹,

Zabludowski²,

Zoccali³

et al. 1984

Brit J Clinical Pharma

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The immediate and long‐term effects of enalapril (MK421) and its lysine analogue (MK521) in once‐daily dosage, were compared in a study of 12 normal subjects. Both compounds lowered blood pressure equally throughout 24 h without causing tachycardia. The biochemical changes with MK521 were more sustained than with MK421, but this did not affect the magnitude of blood pressure reduction. Twenty‐four hours after the previous dose, with both active drugs, plasma renin concentration was significantly higher on day 8 than on day 1, though angiotensin I did not increase in proportion; this probably reflects a fall in renin‐ substrate with prolonged converting enzyme inhibition. There was an early natriuresis with each compound but this effect was no longer apparent after 8 days of continuous therapy. Both MK421 and MK521 were well tolerated with no serious side effects.

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“…A similar effect has been described in normal subjects. 13 Plasma prolactin concentrations were below the limit of reliable estimation ( < 6 0 mU/L) during bromocriptine therapy and during dopamine infusions. Basal prolactin concentrations at other times were normal, as were prolactin responses to metoclopramide (data not shown).…”

Section: Acth Ng/kg/nlnmentioning

confidence: 99%

“…13 Basal aldosterone secretion is increased 2 and aldosterone response to adrenocorticotropic hormone (ACTH) is exaggerated, 4 but the exact cause of these biochemical abnormalities, and indeed of the hypertension itself, remains a matter for speculation. 56 We studied two brothers with this condition and examined the effect of dexamethasone therapy on body sodium and potassium content.…”

Section: Examethasone-suppressible Hyperaldo-imentioning

confidence: 99%

Dexamethasone-suppressible hyperaldosteronism. Adrenal transition cell hyperplasia?

Connell¹,

Kenyon²,

Corrie³

et al. 1986

Hypertension

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SUMMARY Dexamethasone-suppressible hyperaldosteronism is a rare familial syndrome in which hypokalemia, suppression of plasma renin concentration, and elevated aldosterone secretion are corrected by treatment with glucocorticoids. Regulation of adrenocortical function and body electrolytes was studied in two affected brothers. Both were hypertensive (210/128 and 160/106 mm Hg) with hypokalemia (3.3 and 3.5 mM) and low plasma renin concentrations. Aldosterone was elevated intermittently with levels as high as 45 ng/dl (normal range, 4-16 ng/dl). Cortisol concentrations were normal but were correlated with aldosterone levels (r = 0.9 and 0.7). Concentrations of 11-deoxycorticosterone (19 and 21 ng/dl; normal range, 4-16 ng/dl) and 18-hydroxycortisol (1000 and 950 ng/dl; normal range, 34-150 ng/dl) were elevated, and diurnal changes in both were the same as those seen with aldosterone. Infusion of adrenocorticotropic hormone,_ 24 (ACTH) caused exaggerated increases of aldosterone, 11-deoxycorticosterone, and 18-hydroxycortisol; cortisol response was normal. A 4-week trial of dexamethasone normalized blood pressure and caused a natriuresis, a fall in aldosterone, and a rise in plasma renin. Administration of ACTH after dexamethasone treatment again caused exaggerated increases of aldosterone. Aldosterone did not respond to angiotensin II before dexamethasone therapy (r = 0.01), but it showed a normal response after therapy (r = 0.8, p<0.01). Neither administration of dopamine (1 /xg/kg/min) nor long-term therapy with bromocriptine (2.5 mg t.i.d. for 4 weeks) affected aldosterone biosynthesis. Thus, loss of dopaminergic inhibition of mineralocorticoid biosynthesis does not account for hyperaldosteronism in this condition. The abnormal pattern of steroid secretion in these brothers is consistent with a population of adrenocortical transition-type cells that secrete aldosterone in response to ACTH but not to angiotensin II and have biosynthetic characteristics of both zona glomerulosa and zona fasciculata cell types. These properties would explain the excess synthesis of 18-hydroxycortisol from a cell type that can uniquely hydroxylate steroid at both the 17 and 18 positions. (Hypertension 8: 669-676, 1986) KEY WORDS • hyperaldosteronism • cortisol • 18-hydroxycortisol 11-deoxycorticosterone * corticosterone EXAMETHASONE-suppressible hyperaldo-I I steronism is a familial form of hypertension A.^^ in which features of mineralocorticoid excess (hypokalemia, low plasma renin concentration) and elevated blood pressure remit during glucocorticoid treatment.13 Basal aldosterone secretion is increased 2 and aldosterone response to adrenocorticotropic hormone (ACTH) is exaggerated, 4 but the exact cause of these biochemical abnormalities, and indeed of the Received September 18, 1985; accepted January 28, 1986. hypertension itself, remains a matter for speculation. 56We studied two brothers with this condition and examined the effect of dexamethasone therapy on body sodium and potassium content. We also examined the effe...

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A Comparison of Double-Isotope Derivative and Radioimmunological Estimation of Plasma Aldosterone Concentration in Man

Cited by 76 publications

References 5 publications

(+)‐sulpiride antagonises the renal effects of gamma‐L‐glutamyl‐L‐dopa in man.

(+)‐sulpiride antagonises the renal effects of gamma‐L‐glutamyl‐L‐dopa in man.

Enalapril (MK421) and its lysine analogue (MK521): a comparison of acute and chronic effects on blood pressure, renin‐angiotensin system and sodium excretion in normal man.

Dexamethasone-suppressible hyperaldosteronism. Adrenal transition cell hyperplasia?

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