Hyporeninemic hypertension

Crane, Milton G.; Harris, Jennifer; Johns, Varner J.

doi:10.1016/0002-9343(72)90036-8

Cited by 134 publications

(27 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Now, one of the topics of hypertension research is on low renin essential hypertension. In patients with essential hypertension , about 20% have relatively low plasma renin activity and fail to increase it normally in response to sodium restriction and standing (Brunner et al 1972;Crane et al . 1972 In low renin essential hypertension, two types of kallikrein excretion were observed.…”

Section: Discussionmentioning

confidence: 99%

Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism.

Seino

Abe

Sakurai

et al. 1977

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism.

Seino

Abe

Sakurai

et al. 1977

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

“…Approximately 25% of patients with essential hypertension have suppressed renin activity (14,(22)(23)(24)(25), and some investigators have suggested that these patients are volume-expanded (22,26,27). Since increased secretion of aldosterone is found in only a small fraction of these patients, secretion of other mineralocorticoid-like steroids has been assessed.…”

Section: Discussionmentioning

confidence: 99%

The regulation of plasma 18-hydroxy 11-deoxycorticosterone in man.

Williams¹,

Braley²,

Underwood³

1976

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T 18-hydroxy 11-deoxycorticosterone (18-OH DOC), a weak mineralocorticoid, was estimated by a radioimmunoassay procedure after purification in 49 patients with hyper,tension and 38 normal control subjects. The sensitivity of the method was 2-4 pg; there was no detectable blank, and the precision was 9-10%. In normal subjects the absolute plasma levels were similar to those of aldosterone. ACTH administration produced a 23-fold increase, and sodium restriction resulted in a 4-fold increase (5.4+-0.7-20.5±3.0 ng/dl). On the other hand, the plasma levels of 18-OH DOC declined by nearly 50% with upright posture or angiotensin II infusion. During both of these procedures, plasma aldosterone levels significantly increased. Patients with normal and low renin hypertension had similar changes in plasma 18-OH DOC levels with sodium restriction. However, the mean high sodium level in the normal renin essential hypertension group (11.6±-1.6 ng/dl) was significantly greater (P < 0.001) than in the control group (5.4±0.7 ng/dl). In addition, at least 22% and perhaps as high as 37% of the hypertensive subjects had levels greater than the upper limits of normal on a high sodium intake. Differences between the groups were less impressive in the sodiumrestricted studies. There were no significant differences in age, duration of hypertension, sodium balance, serum sodium, potassium, or blood urea nitrogen in those patients who had elevated levels of plasma 18-OH DOC. Patients with primary aldosteronism had levels within -the normal range on both dietary intake. However, in contrast to the other groups there were no significant changes in the plasma levels with sodium restriction. Thus, a significant number of patients with essential hypertension presumably have an alteration in 18-OH DOC secretion.

show abstract

“…2). Mean values for the 10 plasma cortisol samples (5 determinations each in the 2 patients) during the control period were not significantly dif- FIGuRE 2 Plasma concentrations of selected steroids in two patients with low renin essential hypertension before (control) and again 4 (26,27). The gradual lowering of' blood pressure an(d body weight during aminoglutethimide therapy in our low renin patients is also conisistent with the view that the antihypertenisive eff'ect of' the drug is mediated through a reduction in extracellular fluid volume, probably secondary to the sustained suppression of' aldosterone production (Table I).…”

Section: Methodsmentioning

confidence: 99%

“…In all patients aldosterone concentrations in plasma and urine were within normal limits before the study. Mean (2)(3)(4)(5). The finding that low renin hypertension was present in 9-50% of hypertensive patients, depending upon the age of the population studied (6, 7), generated considerable interest in the pathophysiologic mechanisms which might contribute to a low plasma renin.…”

mentioning

confidence: 99%

Effect of Aminoglutethimide on Blood Pressure and Steroid Secretion in Patients with Low Renin Essential Hypertension

et al. 1978

View full text Add to dashboard Cite

A B S T R A C T An inhibitor of adrenal steroid biosynthesis, aminoglutethimide, was administered to seven patients with low renin essential hypertension, and the antihypertensive action of the drug was compared with its effects on adrenal steroid production. In all patients aldosterone concentrations in plasma and urine were within normal limits before the study. Mean The gradual lowering of blood pressure and body weight during aminoglutethimide therapy is consistent with the view that the antihypertensive effect of the drug is mediated through a reduction in the patients' extracellular fluid volume, probably secondary to the persistent decrease in aldosterone production. The observation that chronic administration of aminoglutethimide lowered blood pressure in these patients and elevated their plasma renin activity to the normal range without decreasing production of the adrenal steroids, deoxycorticosterone, 18-hydroxydeoxycorticosterone, and 16,3-hydroxydehydroepiandrosterone, makes it unlikely that these steroids are responsible either for the decreased renin or the elevated blood pressure in patients with low renin essential hypertension.

show abstract

Hyporeninemic hypertension

Cited by 134 publications

References 28 publications

Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism.

Effect of spironolactone on urinary kallikrein excretion in patients with essential hypertension and in primary aldosteronism.

The regulation of plasma 18-hydroxy 11-deoxycorticosterone in man.

Effect of Aminoglutethimide on Blood Pressure and Steroid Secretion in Patients with Low Renin Essential Hypertension

Contact Info

Product

Resources

About