Abstract
Low-renin hypertension (LREH) accounts for an important subset of the hypertensive human population and is associated with salt-sensitivity and diuretic response and is also common in black patients. An interesting finding in LREH is the presence of normal plasma aldosterone levels.1 2 The ratio of plasma aldosterone to renin activity is used to screen for adrenal adenomas and hyperplasia3 and is usually >100 when plasma renin activity is expressed in ng/mL/hr and the aldosterone concentration is expressed in ng/dL. The plasma aldosterone/plasma renin activity ratios may be somewhat elevated in LREH (>30 but <100), which is especially relevant if the concurrent urinary sodium excretion exceeds 200 mEq/24 hours.4 It is not known what regulates aldosterone secretion in this setting or whether there is actual mineralocorticoid excess. Undue prior emphasis may have been placed on the continued suppression of plasma renin activity during severe salt restriction or volume depletion in LREH,1 and the suppression of plasma renin activity and basal aldosterone secretion5 in the elderly can also confound the analysis of LREH. Studies by Fisher et al2 focus on adrenal and pressor responsiveness to angiotensin II (Ang II) as a function of dietary salt intake in patients with LREH, normal-renin hypertension, and normal controls. Especially striking are the functional similarities between LREH and “ nonmodulating” essential hypertension with normal plasma renin activity (NMEH), including: (1) salt-sensitivity of the blood pressure; (2) blunted plasma aldosterone responses to Ang II infusion and upright posture after 5 days of rigid dietary sodium restriction; and (3) relatively low basal plasma aldosterone levels. These differences compared with normal controls and “modulating” hypertensive subjects disappeared when the dietary salt intake was increased to 200 mEq. The latter results are consistent with suppression of plasma Ang II activity during high-salt intake with …
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