The assessment of potassium (K) effects in hypertension involves a history of complex research in cell K function and body K homeostasis. These studies provide evidence for the role of K ions in vascular and renal function, insulin resistance, glucose uptake, and the renin-angiotensin-aldosterone system; and there have been an impressive number of clinical and epidemiologic research relating dietary intake K and regulation of blood pressure. However, the usual technique by which K metabolism is assessed in clinical practice (plasma or serum K) provides no useful data for estimating disorders in cell K transport that occurs in hypertensive patients or that may follow the administration of diuretics, beta-blockers, or nonsteroidal anti-inflammatory drugs. This fact becomes more crucial if associated with the physiologic decline in body K stores occurring after the age of 30 years, which may impair the long-term treatment of hypertensive individuals. In this context, this article presents a review of the clinical and research methods that can be used to assess more accurately K metabolism and cell K physiology in hypertensive patients, including a heritable defect in red blood cell K transport.