1. Pronounced hypoaldosteronism was found in five young women with low-renin hypertension and characteristic features of the mineralocorticoid hypertensive syndrome. 2. There was no overproduction of the mineralocorticoids 11-deoxycorticosterone and 18-OH-11-deoxycorticosterone. 3. Dexamethasone restored blood pressure to normal, decreased body weight, increased plasma potassium, and increased plasma renin activity and aldosterone excretion in all patients. 4. The data suggest overproduction of an unknown adrenocorticotrophic hormone-dependent mineralocorticoid maintaining hypertension in these patients.

1. Indomethacin was administered alone or in addition to either diuretic or propranolol therapy to three groups of patients with essential hypertension on a free sodium diet. 2. Indomethacin administration reduced renin secretion by about 30% in untreated uncomplicated hypertensive patients and by about 75% in those whose renin secretion had either been stimulated or suppressed by maintained diuretic or β-adrenoreceptor-blockade therapy. 3. Indomethacin administration produced no net effect on blood pressure in untreated patients with uncomplicated hypertension but it blunted or reversed the antihypertensive effect of either diuretic or propranolol therapy. 4. Salt and water retention may be an important factor in the blood pressure-raising effect of indomethacin during diuretic or propranolol therapy: In addition, prostaglandin synthesis may be important in counteracting increased α-adrenergic tone, which may limit the blood pressure-lowering effect of β-adrenoreceptor-blockade. 5. Because of these interactions and their pressor potential indomethacin should be used with caution when combined with either diuretics or β-adrenoreceptor blockers.

1. Three renin-stimulating methods for detection of low-renin hypertension have been compared. First, renin activity was measured in hospital patients after 5 days of sodium restriction and 3 h ambulation. Secondly, renin activity was measured after frusemide stimulation [0.42 mmol (140 mg) in 18 h] and 3 h ambulation. Thirdly, renin activity was measured after 5 days of chlorthalidone treatment [0.3 mmol (100 mg)/day] and 3 h ambulation. The last two tests were done with the subjects as out-patients without any dietary regimen. 2. In eleven normotensive control subjects and twenty hypertensive patients the results after frusemide were not comparable with those after sodium restriction since the frusemide test did not identify the same renin-suppressed hypertensive subjects as the sodium-restriction procedure. 3. After 5 days of chlorthalidone treatment the renin values in eleven control subjects as well as in thirty-eight hypertensive patients were significantly higher than after sodium restriction. The values obtained after each procedure were closely correlated. 4. Thus the out-patient chlorthalidone procedure identified similar sub-groups of patients as having low- or normal-renin hypertension as did the in-patient sodium-restriction test.