The prevalence of primary aldosteronism (PA) in patients with hypertension has been widely disputed since the syndrome was first described by Jerome W. Conn in 1956. It was originally believed to be rare, but in 1964 Dr. Conn noted that 2 hallmarks of PA, low plasma renin activity (PRA) and adrenal adenomas, were present in many hypertensive persons. He suggested that the prevalence of PA, rather than less than 1%, might be as high as 20% (1).
Within the next few years, low PRA levels were indeed noted in hypertensive patients (2). Increased mineralocorticoid activity was suspected in these patients because of low salivary sodium–potassium ratios, a marker of mineralocorticoid excess (3), and an exaggerated decrease in blood pressure after treatment with aminoglutethimide, a blocker of adrenal steroid hormone production (4), and with spironolactone, an inhibitor of the mineralocorticoid receptor (5). But urinary aldosterone excretion was normal in these patients, so researchers postulated that the suspected mineralocorticoid excess was caused by an unknown mineralocorticoid or by aldosterone, despite its normal levels.