How do plasma renin activity and aldosterone secretion respond to varying sodium intake and chlorothiazide in hypertensive patients?
The study identifies a subset of essential hypertension patients with low plasma renin activity who fail to mount a normal renin-aldosterone response to sodium depletion and diuretics, putting them at risk for hyponatremia and postural hypotension.
Plasma renin activity (PRA) and aldosterone secretion or excretion rates have been measured in 35 hypertensive patients. Most hypertensive patients respond normally to decreased sodium intake and upright posture with an increase in PRA, which is further enhanced when chlorothiazide is given. PRA was found to be above the normal range in malignant hypertension and in some patients with renovascular and essential hypertension. PRA remained increased for up to 2 months after taking estrogen and progestin. Subnormal PRA has been observed in primary aldosteronism and Cushing's syndrome. Six patients with essential hypertension had low PRA. When these patients were given a low sodium diet and chlorothiazide, neither PRA nor aldosterone increased normally, urinary sodium loss continued, and hyponatremia developed in 3 of the 6 patients. Postural hypotension was observed in 5 of the 6 cases during sodium depletion. Aldosterone secretion was well correlated with PRA in most hypertensives. Exceptions were noted in primary aldosteronism, Cushing's syndrome, and after administration of chlorothiazide. The fraction of labeled aldosterone excreted as acid-labile conjugate was within normal limits.
Weinberger et al. (1968) studied this question.