Elevation of Plasma Levels of ACTH and Aldosterone in Patients with Essential Hypertension; Possible Roles in Low Renin Hypertension
Yuji MizunoHirofumi YasueMichihiro YoshimuraEisaku HaradaHiromi FujiiShota NakamuraTeruhiko ItohMegumi YamamuroHisao Ogawa
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Plasma renin activity
Essential hypertension
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Low renin hypertension probably does not represent a clinical entity. In many patients with low renin hypertension blood pressure is normalized by treatment with diuretics only; in these patients a (genetic?) sensitivity to salt might play a predominant role in the pathogenesis of hypertension and renin suppression. In another group of patients renin suppression appears to be secondary to the hypertensive process. This is indicated by the observation that prevalence of low renin hypertension increases with age and that it is more frequent in advanced stages of hypertension. Also a diminished sympathetic tone might play a part in the renin unresponsiveness. Finally, although no positive evidence was found, the possibility cannot be excluded that, at least in some cases, a mineralocorticoid other than aldosterone is involved. Neither in normotensive subjects nor in hypertensive patients, both with normal and with low plasma renin was a correlation between plasma renin concentration and plasma aldosterone concentration following stimulation by upright posture found. More detailed studies will be necessary to clarify the relationship between the renin-angiotensin system and aldosterone secretion during upright posture, in particular in patients with low renin hypertension.
Plasma renin activity
Pathophysiology of hypertension
Mineralocorticoid
Pathogenesis
Essential hypertension
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Essential hypertension
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Pathogenesis
Plasma renin activity
Essential hypertension
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Essential hypertension
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Primary Aldosteronism
Mineralocorticoid
Essential hypertension
Plasma renin activity
Pathophysiology of hypertension
Hyperaldosteronism
Secondary hypertension
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Enhanced Adrenal Responsiveness to Angiotensin II in Patients with Low Renin Essential Hypertension*
The plasma aldosterone response to infused angiotensin II was determined in normal controls and in patients with normal renin and with low renin essential hypertension. The patients with low renin essential hypertension showed an enhanced plasma aldosterone response when compared to the other two groups. This finding may explain why plasma aldosterone levels remain within normal limits in the face of suppressed plasma renin and angiotensin II concentrations in low renin essential hypertension. (JClin Endocrinol Metab 48: 266, 1979)
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The possibility that an abnormality of aldosterone metabolism plays a role in the pathogenesis of low-renin essential hypertension was investigated. Normal subjects and patients with low-renin or normal-renin essential hypertension were evaluated while in balance, ingesting a diet providing 120 mEq sodium and 70 mEq potassium. Aldosterone metabolic clearances were determined by a constant infusion technique using tritiumlabeled aldosterone. Aldosterone secretion rates and plasma aldosterone concentrations were measured by radioimmunoassay. Aldosterone metabolic clearance in normal subjects was 1422 ± 69 (mean ± SE) liters/24 hours. In patients with low-renin essential hypertension, aldosterone metabolic clearance was 1351 ± 61 liters/24 hours, and in patients with normal-renin essential hypertension, it was 1412 ± 66 liters/24 hours. These values were not significantly different from those of normal subjects. Although aldosterone secretion rates in both groups of hypertensive patients were within the normal range, patients with low-renin essential hypertension, under the conditions of this study, had significantly higher secretion rates than patients with normal-renin essential hypertension. We have concluded that the maintenance of plasma aldosterone in low-renin essential hypertension reflects sustained aldosterone secretion despite suppression of plasma renin activity, rather than reduced aldosterone metabolism. The maintenance of normal aldosterone secretion in low-renin essential hypertension appears to be inappropriate and is not explained by alterations of known regulatory mechanisms.
Plasma renin activity
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Pathophysiology of hypertension
Hyperaldosteronism
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1. The renin-aldosterone system was studied in seventy-one selected hypertensive patients. Nine (13%) were diagnosed as having primary aldosteronism. Of the twenty-three patients who presented with a history of unprovoked hypokalaemia, the incidence of primary aldosteronism was 40%. 2. Renin and aldosterone responses to the combined stimuli of a low sodium diet and the upright posture were suppressed in patients with essential hypertension. There was no evidence that the suppression was due to abnormal adrenal function, sympathetic neuropathy, or the level of the blood pressure. The mechanism of the suppressed plasma renin activity response and its significance in the pathogenesis of hypertension are unknown.
Primary Aldosteronism
Plasma renin activity
Essential hypertension
Pathogenesis
Hyperaldosteronism
Pathophysiology of hypertension
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