In the syndrome of hyperaldosteronism, the abnormal electrolyte metabolism, secondary to mineralocorticoid excess, seems to play a predominant pathogenetic role in causing elevation of the blood pressure, since the renin-angiotensin system is depressed and unresponsive. The available evidence (results of treatment, consistent failure to cause high blood pressure by administration of excessive salt-remaining steroids to normotensive volunteers, the salt-hypertension model in experimental animals, the higher incidence of adrenal adenomas in hypertensive patients, etc.), however, suggests that other factors participate in the mechanism of hypertension. Angiotensin II stimulates aldosterone secretion, thereby affecting electrolyte balance; in addition, this polypeptide is the most powerful vasoconstrictor known today, the effectiveness of which is greater in a Na-replete condition. In some hypertensive states (renovascular hypertension, end-stage renal disease, malignant phase hypertension, hypertension related to oral-contraceptive medication, and primary reninism) both the renin-angiotensin system and aldosterone production may be elevated. In this group, however, correlation between the latter two variables and hypertension is not sufficiently consistent to implicate them as the sole pathogenetic factors. In the larger group of patients with essential hypertension, the renin-angiotensin-aldosterone system and electrolyte metabolism range from normal to subtle changes (depressed plasma renin, incomplete aldosterone suppression by salt load, decrease in aldosterone metabolism, exaggerated natriuresis, reversal of electrolyte circadian cycle) of difficult interpretation. We suggest that the same factors, clearly abnormal in hypertensive states of more defined etiology, are also at play in causing essential hypertension, perhaps through some as yet undefined abnormal interrelationship.