Clinical, biochemical and pathological features of low-renin (“primary”) hyperaldosteronism

Ferriss, J. B.; Beevers, D. G.; Brown, J. J.; Davies, David; Fraser, Robert; Lever, A. F.; Mason, P A; Neville, A. Munro; Robertson, J. I. S.

doi:10.1016/0002-8703(78)90370-8

Cited by 98 publications

(32 citation statements)

References 74 publications

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“…We should also comment on the aldosterone increments that occurred on assumption of upright posture in our patients with unilateral adrenal mass in contrast to the ACTH-mediated circadian declines commonly referred to as typical of that condition. 16 We believe that the discrepancy is only apparent because our aldosterone samples were withdrawn at at time when ACTH-and plasma cortisol-not only did not show circadian falls, but actually increased (probably as a consequence of stress-related phenomena during the sampling procedure), thus providing an effective stimulus for adenomatous adrenal tissue.…”

Section: Discussionmentioning

confidence: 90%

“…Although our controls were not exactly matched for age, blood pressure, and dietary sodium intake with patients, the results are suggestive of elevated basal ANF values in PA, in agreement with other reports 10 ' " and consistent with an increased secretion compensatory to the expanded body fluid volume peculiar to PA. 16 Furthermore, ANF responded to long-term changes in dietary sodium content by decreasing and increasing appropriately, at variance with the otherwise expected insensitivity of plasma aldosterone to those maneuvers. Furthermore, concordant with some 7 -M but not all 29 -r esults in normal subjects, 1 hour of standing, possibly through central fluid volume redistribution 31 and atrial decompression, 32 was associated with ANF decrements.…”

Section: Discussionmentioning

confidence: 96%

“…The diagnosis of PA was based on suppressed plasma renin activity (PRA) values (ranging from 0.09-0.16 ng/angiotensin I [Ang I]hr), high urinary aldosterone excretion (range, 38-150 /xg/24 hr), and hypokalemia (range, 2.0-3.2 mmol/L). Three patients were considered to have bilateral hyperplasia based on the presence of postural increments in plasma aldosterone 16 and visualization of normal adrenals on computed tomographic scans. The five others showed circadian plasma aldosterone falls from 0800 to 1200 16 and unilateral adrenal masses on computed tomographic scan.…”

Section: Methodsmentioning

confidence: 99%

“…Three patients were considered to have bilateral hyperplasia based on the presence of postural increments in plasma aldosterone 16 and visualization of normal adrenals on computed tomographic scans. The five others showed circadian plasma aldosterone falls from 0800 to 1200 16 and unilateral adrenal masses on computed tomographic scan. Therefore, a diagnosis of aldosterone-secreting adrenal adenomas was posed, although it was confirmed surgically in only one of them since the remaining four patients refused an operation.…”

Section: Methodsmentioning

confidence: 99%

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Dietary sodium change in primary aldosteronism. Atrial natriuretic factor, hormonal, and vascular responses.

et al. 1988

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SUMMARY Atria] natriuretic factor (ANF) may be physiopathotogkally involved in several clinical conditions including human hypertension. However, few data are available regarding this putative hormone and its relationship to aldosterone, blood pressure, and vascular responsiveness to a-adrenergic receptor stimulation in primary aldosteronism, a volume-expanded, low-renin model of human hypertension. For this reason, the behavior of supine and upright plasma ANF as related to aldosterone, blood pressure, and forearm a-adrenergk sensitivity (plethysmographic technique) to intra-arterial norepinephrine infusion was studied in eight patients with primary aldosteronism (five with adenomas, three with hyperplasia) before and at the end of two sequential 1-week low (20 mmol/day) and high sodium (200 mmol/day) diet periods. Basal, prediet ANF concentrations decreased and increased after low and high sodium intakes, respectively. Furthermore, highly significant postural ANF decrements after 1 hour of standing occurred with each diet, although they were lower after the low than after the high sodium diet. Plasma aldosterone, either supine or upright, was insensitive to dietary sodium manipulations, suggesting the absence of ANF-mediated control of aldosterone secretion in our patients. In spite of about twofold higher ANF concentrations during the high than during the low sodium diet, forearm vascular sensitivity to intra-arterial norepinephrine infusion did not change during the study. Furthermore, systemic arterial blood pressure rose to a highly significant extent after dietary sodium content was increased, thus casting doubt on a role for ANF as an endogenous long-term modulator of systemic blood pressure and peripheral a-adrenergk sensitivity in patients with primary aldosteronism. (Hypertension 12: 192-198, 1988) KEY WORDS • atrial natriuretic factor a-adrenergk sensitivity blood pressure • sodium * primary aldosteronism S INCE the first reports describing the existence of secretory granules in mammalian atria, 12 the biochemical nature of a circulating atrial natriuretic factor (ANF) has been studied, its natriuretic, vasodilating, aldosterone-inhibiting, and aadrenergic antagonistic properties have been identified (for a review, see References 3-5), and its dependence on acute and chronic changes in body fluid volume status has been characterized in normal humans.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 96%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Dietary sodium change in primary aldosteronism. Atrial natriuretic factor, hormonal, and vascular responses.

et al. 1988

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“…All had a normal intravenous pyelogram and were without clinical or biochemical evidence of Cushing's syndrome or phaeochromocytoma. Hypertensive patients were considered in four groups: GROUP I Twenty-eight patients had primary hyperaldosteronism with an adrenal adenoma (Conn's syndrome) confirmed in each by surgery and histological examination of the adrenal cortex (Ferriss et al, 1978a and b). Other findings are given in Table 1 and in Davies et al (1979).…”

Section: Methodsmentioning

confidence: 99%