Are Idiopathic Hyperaldosteronism and Low-Renin Hypertension Variants of Essential Hypertension?

Brown, J. J.; Lever, A. F.; Robertson, J. I. S.; Beevers, D. G.; Cumming, A. M. M.; Davies, David; Fraser, Robert; Mason, P A; Morton, J.

doi:10.1177/000456327901600196

Cited by 20 publications

(12 citation statements)

References 27 publications

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“…In contrast to normal subjects, plasma aldosterone concentrations follow changes in ACTH secretion more closely than those of plasma angiotensin I1 Kern et al, 1978; Espiner & Donald, 1980). Indeed, as might be predicted in any syndrome of primary hormone excess, plasma aldosterone concentration is inversely proportional to that of its trophin, angiotensin I1 (or renin) (Davies et al, 1979). …”

mentioning

confidence: 86%

“…However, about 10% of cases may be normokalaemic and, in others, hypokalaemia may be intermittent (Davies et al, 1979;Ferriss et at., 1978). Total body (or total exchangeable) electrolyte measurements may be less ambiguous.…”

Section: Primary Hyperafdosteronismmentioning

confidence: 99%

“…Indeed, similar adrenal pathology has been described in patients with essential hypertension at autopsy (Longo et al, 1978). Also, in idiopathic hyperaldosteronism, there is a direct relationship between basal plasma angiotensin I1 (or renin) and aldosterone concentrations (Davies et al, 1979) suggesting that hypersecretion is not 'primary'. It is therefore clear that primary and idiopathic hyperaldosteronism are different disorders, despite qualitatively similar biochemical disturbances, and it has been suggested that the latter condition may be a variant of 'low renin' essential hypertension Fraser & Padfield, 1985).…”

Section: Idiopathic Hyperaldosteronismmentioning

confidence: 99%

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Hormones and Hypertension

Fraser

Davies

Connell

1989

Clinical Endocrinology

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The importance of changes in hormone secretion in human hypertension is a complex problem and too large to be dealt with in uniform detail in a short review. The subject encompasses not only the effects on blood pressure of primary endocrine disorders but also hormonal changes secondary to increased blood pressure. Some aspects are more fully understood than others and have been the subjects of relatively recent detailed reviews. Where this is the case, the current review has summarized the present position and cited reviews and key papers, in order to reserve space for more controversial and less well understood conditions such as the hypertension of growth hormone, thyroid hormone or glucocorticoid excess. CORTICOSTEROIDSThe human adrenal cortex synthesizes and secretes a large number of steroid hormones, biosynthetically interrelated with each other and with qualitatively and quantitatively different biological activities. The two major categories of compound are the adrenal androgens (androstenedione, dehydroepiandrosterone and testosterone) which, as far as is known, are not important in blood pressure control and will not be considered further (although there exist experimental models of hypertension which may be androgendependent), and the corticosteroids. These C21 steroids of the pregnane series exert two main types of action, mineralocorticoid and glucocorticoid effects, and excess secretion of either has widespread repercussions, particularly for neuromuscular function and the control of salt and water metabolism. Mineralocorticoids act mainly on the distal nephron via specific receptor activation to promote sodium reabsorption (with associated changes in extracellular fluid and plasma volume) and increased potassium and proton excretion, so that excess activity is characterized by hypokalaemia and a metabolic alkalosis. Aldosterone is the major mineralocorticoid in man but deoxycorticosterone (DOC) and corticosterone also have significant activity. More recently discovered compounds-18-hydroxy DOC, 18-oxocortisol and several compounds modified at position 19 (19-hydroxy or 19-nor)-may also contribute to the total mineralocorticoid action of the adrenocortical secretion (see review by Fraser & Padfield, 1985). Cortisol is the major human glucocorticoid. Glucocorticoids promote liver glycogen and protein synthesis but are catabolic in most other tissues, increasing lipolysis and protein R. Fraser et al.breakdown and reducing glucose uptake from the circulation. However, the kidney also possesses specific glucocorticoid receptors and, under experimental conditions, glucocorticoids can be shown to promote both natriuresis and kaliuresis, at least partly by raising glomerular filtration rate (GFR) and also to modulate Na+-H+ exchange in the proximal nephron (Davis & Howell, 1953;Mahnensmith & Aronson, 1985; Kinsella et al., 1985). Excess of either mineralocorticoid or glucocorticoid activity is associated with hypertension.The control of adrenocortical function is similarly complex and the subject of sev...

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confidence: 86%

Section: Primary Hyperafdosteronismmentioning

confidence: 99%

Section: Idiopathic Hyperaldosteronismmentioning

confidence: 99%

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Hormones and Hypertension

Fraser

Davies

Connell

1989

Clinical Endocrinology

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“…There is, however, no evidence that aldosterone-secreting adenomas are more common in Black patients when compared with White patients. Possibly nontumor 'idiopathic hyperaldosteronism' is more common in Black patients, although the nature and existence of this disease is open to debate [36,37].…”

Section: Secondary Hypertensionmentioning

confidence: 99%

Hypertension in ethnic groups: epidemiological and clinical perspectives

Dwivedi

Beevers

2009

Expert Review of Cardiovascular Therapy

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In the UK and other developed nations, hypertension and its vascular complications are more common in ethnically African and South-Asian communities compared with Europeans. While these conditions are less common in rural India and Africa, they present a rising problem in expanding cities in all developing countries. Hypertension is, therefore, mainly related to environmental and lifestyle factors rather than genetically determined racial differences. Studies in the USA and elsewhere show that the striking differences in the prevalence of hypertension between people of African and European origin are greatly reduced after adjustment for socio-economic status. One important and probably genuine racial difference between ethnic groups is the significantly suppressed activity of the renin-angiotensin-aldosterone system in African-origin hypertensive patients. As a consequence of this, they are rather more sensitive to a low-salt diet but significantly less sensitive to drugs that block the renin-angiotensin-aldosterone system (angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers) and beta-blockers. There is also evidence that renin suppression is common in Japanese and Chinese hypertensive patients as well, although no direct comparisons between these two groups with European-origin patients have been carried out. The management and control of hypertension is unsatisfactory in all ethnic groups and all nations. No one group needs particular targeting; all need better quality systematic care.

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“…33 This finding questioned the validity of IHA as a distinct diagnostic entity, 34 and there was even a suggestion that hyperaldosteronism plays no part in maintaining hypertension in this PA subgroup. 35 Whilst it is undeniable that at one end of the spectrum of IHA cases, the clinical and laboratory features of hyperaldosteronism are clearly present, the lack of an expanded body sodium in some IHA cases is an apparent paradox which can be explained.…”

Section: The Controversy Of Idiopathic Hyperaldosteronismmentioning

confidence: 99%

Is aldosterone the missing link in refractory hypertension?: aldosterone-to-renin ratio as a marker of inappropriate aldosterone activity

2002

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Use of the random aldosterone-to-renin ratio (ARR) as a reliable marker of inappropriate aldosterone activity has led to primary aldosteronism (PA) being increasingly diagnosed in hypertensive patients. At least 10% of hypertensives have been found to have PA, the majority of whom presumably have bilateral adrenal hyperplasia or idiopathic hyperaldosteronism as an aetiology for PA. Whilst these patients clearly have excess aldosterone activity, they have in common many features that are found in hypertensive patients in general, amongst which include heightened angiotensin II adre-

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Are Idiopathic Hyperaldosteronism and Low-Renin Hypertension Variants of Essential Hypertension?

Cited by 20 publications

References 27 publications

Hormones and Hypertension

Hormones and Hypertension

Hypertension in ethnic groups: epidemiological and clinical perspectives

Is aldosterone the missing link in refractory hypertension?: aldosterone-to-renin ratio as a marker of inappropriate aldosterone activity

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