Key result
Low-renin essential hypertension was associated with normal aldosterone metabolic clearance (1351 +/- 61 liters/24 hours) compared to normal subjects (1422 +/- 69 liters/24 hours).
Why the study?
Is aldosterone metabolic clearance altered in patients with low-renin essential hypertension compared to normal subjects or those with normal-renin essential hypertension?
Observational
Is aldosterone metabolic clearance altered in patients with low-renin essential hypertension compared to normal subjects or those with normal-renin essential hypertension?
Absolute Event Rate: 1351% vs 1422%
p-value: p=not significantly different
Aldosterone metabolic clearance is normal in low-renin essential hypertension, indicating that maintained plasma aldosterone levels reflect sustained secretion rather than reduced metabolism.
Normal aldosterone clearance in low-renin hypertension should not change practice; supports sustained secretion but remains hypothesis-generating.
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 tritium-labeled 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.
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Ronald D. Brown (1976) conducted an observational in Low-renin essential hypertension. Low-renin essential hypertension vs. Normal subjects and normal-renin essential hypertension was evaluated on Aldosterone metabolic clearance (p=not significantly different). Low-renin essential hypertension was associated with normal aldosterone metabolic clearance (1351 +/- 61 liters/24 hours) compared to normal subjects (1422 +/- 69 liters/24 hours).
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