ABSTRACT
Mineralocorticoids raise blood pressure by increasing salt reabsorption via renal cortical tubular epithelial sodium channels (ENaC), which are highly regulated by the renin-angiotensin system (RAS). Primary aldosteronism, the most striking example of mineralocorticoid excess, is discussed in Chapter 13. Other forms of mineralocorticoid hypertension may be attributed to excessive adrenal mineralocorticoid secretion, an inability to metabolize cortisol to its inactive metabolite, cortisone, or mutations that alter the function of either the glucocorticoid or mineralocorticoid receptor (Box 14.1).
