PRIMARY ALDOSTERONISM (PA) is characterized by overproduction of the mineralocorticoid hormone aldosterone by adrenal glands. According to recent reports, it appears to be the most common cause of secondary persistent hypertension, and may account for about 8~13% of unselected hypertensives [1] and as high as 20% of resistant hypertensives [2,3]. The inappropriately high production of aldosterone causes suppression of plasma renin, sodium retention, hypertension, cardiovascular damage, and potassium excretion [4]. Elevated blood pressure combined with the proinflammatory and profibrotic effects of aldosterone To date, although the genetic basis of familial hyperaldosteronism has been more clearly, the exact pathogenesis of sporadic forms of the disease remains unknown. Among a number of studied susceptibility genes, the aldosterone synthase gene (CYP11B2) is the most commonly studied. The CYP11B2 gene situates on chromosome 8q24.3 and encodes aldosterone synthase, which is the key rate-limiting enzyme for the final stage of aldosterone synthesis pathway and pri-
Original