Blood pressure (BP) is maintained by cardiac output and peripheral vascular resistance that, in turn, are modified by stroke volume, pulse rate, total blood volume, blood viscosity, elasticity of blood vessels, and humoral and neurogenic stimuli. Changes in one or more of these variables by pharmacological, behavioral, physiological, or environmental means normally affect BP only transiently because a variety of homeostatic reflexes, responding to the change, act to maintain a relatively stable mean arterial BP. When a homeostatic mechanism chronically maintains BP at abnormally high levels, it is sometimes due to a surgically or medically correctable condition (e.g., coarctation of the aorta, primary hyperaldosteronism, Cushing’s syndrome, pheochromocytoma, or unilateral renal disease). However, more than 90% of all cases of chronically elevated BP are not secondary to one of these correctable conditions, and are therefore referred to as primary, or essential, hypertension (Whelton & Russell, 1984). The nature of essential hypertension (HBP) has been a topic of controversy for some time (Laragh, 1965). The tendency for an individual to develop HBP often runs in families, and population studies have demonstrated a familial resemblance at all levels of the BP continuum. Environmental stimuli also seem to play a significant role in most cases of HBP (Whelton & Russell, 1984). Predominantly environmental factors that have been implicated in the genesis of HBP are increased ingestion of sodium, excessive caloric intake, and emotional stress. Although BP has been demonstrated to rise in response to diets extremely high in sodium and to fall in response to diets extremely low in sodium, a relationship between dietary salt and HBP still has not been clearly established. Similarly, although weight reduction is often associated with BP reduction, even when dietary sodium and potassium are held constant, obesity is rarely the primary cause of HBP. Acute responses of BP to emotional stress also have not been shown to have a role in the etiology of chronic HBP. The role of other environmental factors (eg., alcohol consumption, cigarette smoking, heavy metal intake, and calcium content of water intake) is also unclear although there is evidence that some role exists in each case (Whelton & Russell, 1984). Because these environmental factors are not mutually exclusive in their influence on BP, the view that HBP has a multifactorial etiology is now gaining wide acceptance.