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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 an...

16 patients out of 53 referred for hypertension were taking oral contraceptives at the time of referral and were studied for blood pressure differentials plasma angiotensinogen levels plasma renin activity (PRA) and aldosterone excretion rates (AER) after cessation of the contraceptive treatment. Of the 11 patients who had normal blood pressure before taking the estrogen-gestagen contraceptives all of them showed reduced blood pressure levels within 1-3 months of stopping the treatment. 5 returned to and maintained normal limits for 6 months or longer while the remaining 6 showed reduced blood pressure levels that remained above the upper normal limits. In the 3 women who were hypertensive before treatment blood pressure fell to control levels after discontinuation. Angiotensinogen (renin substrate) concentration in the plasma of the patients receiving oral contraceptives was 2-5 times normal concentration. This also caused increase in angiotensinogen generation. These levels returned to normal within 3 months of cessation of contraception. PRA and AER were 2 times the normal rates under contraceptive therapy. PRA decreased but remained high in some cases 3 months after the treatment was stopped while AER returned to normal within the same period. It is concluded that oral contraceptives can cause hypertension in some patients and aggravate a pre-existing condition in others. Blood pressure therefore should be followed carefully in patients receiving oral contraceptives.