The pathophysiology of primary aldosteronism still remains unknown. In mRNA and protein levels, overexpression of aldosterone synthase (P-450aldo) is recognized, although abnormalities and defects of DNA and its upper stream have not been detected. Several candidate genes responsible for pathogenesis of primary aldosteronism, such as renin, angiotensin receptor type II, etc., have been proposed, but no decisive genes have been found. A relatively reliable screening for hyperaldosteronism is a determination of the ratio of the plasma aldosterone level to the plasma renin activity. For differentiating several types of aldosteronisms, the simplest test is the response of plasma aldosterone to two hours in an upright posture: plasma aldosterone rises in most patients with idiopathic hyperaldosteronism. In contrast, in cases of autonomous aldosterone-producing tumor, most patients show no response or even a decrease in plasma aldosterone concentration. The size and location of the aldosterone-producing adenoma are determined by using computed tomography.