The measurement of peripheral plasma renin activity during the investigation of hypertension has proved useful in distinguishing between primary and secondary aldosteronism. In primary aldosteronism, plasma renin activity is low and does not increase during the administration of a low sodium diet or after the assumption of an upright posture, effects which are seen in normal subjects.1-3 Conversely, in hypertensive diseases associated with secondary aldosteronism, plasma renin activity is usually high, or may increase abnormally as a result of an upright posture or a reduction in arterial pressure.4-6 While these findings are usual in malignant and renovascular hypertension, plasma renin activity and the rate of aldosterone secretion are rarely increased in benign essential hypertension unless this is complicated by sodium deficiency resulting from salt-losing renal disease or from the administration of diuretics.7
Our patient with hypertension was unusual in that plasma renin activity and aldosterone secretion were