An association between mineralocorticoids and hypertension has been recognized for over 50 years, although the mechanisms involved are not entirely clear. In addition to the hypertension seen in cases of frank mineralocorticoid excess, such as in an aldosterone-producing adenoma, many essential hypertensive patients respond to treatments mitigating mineralocorticoid action, even though circulating levels of these steroids are within normal ranges. It has been a decade since David Bohr hypothesized that a center within the brain, probably in the AV3V area, was responsible for the orchestration of the multiple homeostatic mechanisms controlling blood pressure. It was proposed that the "set point" for such a center was dependent upon intracellular Ca + + and/or another ion content or transport across cell membranes, and was altered by mineralocorticoids and in some forms of genetic hypertension. The focus of this paper is the role of the central nervous system in mineralocorticoid hypertension. The importance of these data resides in the possibility that the central mechanisms involved in mineralocorticoid hypertension may also be operant in the pathogenesis of other forms of hypertension, as well as in the normal control of blood pressure.