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Ten patients with benign essential hypertension were studied after sodium loads and during sodium depletion induced by diet and diuretic. Sodium intake of 400 mEq/day did not produce the expected fall in aldosterone secretion or supine plasma aldosterone concentration, which remained within or above the limits observed in normal men on an intake of 120 mEq of sodium. One patient with suppressed plasma renin activity (PRA), high urinary and plasma aldosterone and normal cortisol, had bilaterally enlarged adrenals containing small cortical nodules. Five other patients had low PRA, which did not rise normally on standing or during sodium deprivation, but could be stimulated by further diuretic-induced sodium loss. Two of these 5 cases, studied on a high sodium intake, had trivial increases in plasma aldosterone after standing, but the others had large postural increases without significant change in PRA, plasma cortisol, or plasma sodium or potassium concentration. PRA, aldosterone secretion rate and plasma aldosterone concentration increased during sodium depletion. A large rise in plasma aldosterone was observed in the sodium-depleted hypertensive patients after 4 hr of standing and quiet ambulation. The increases in aldosterone secretion rate and plasma aldosterone concentration following sodium deprivation and standing were generally well correlated with increased PRA. The plasma aldosterone concentrations found in sodium-loaded hypertensives are not readily explained on the basis of regulation by the renin-angiotensin system, and deserve further critical study.
Luetscher et al. (Wed,) studied this question.