The following concept of the pathogenesis of essential hypertension is proposed: there may be a continuous spectrum of noradrenergic sensitivity in normal subjects which is not only inherited but also modified later by different levels of psychological stress or by different types of behavior. The higher the noradrenergic sensitivity in a given subject, the greater the salt sensitivity and the greater the likelihood that hypertension will develop in later life if the usual high sodium-low potassium diet is consumed. Noradrenergic hypersensitivity may be linked to salt sensitivity in that it causes enhanced proximal tubular sodium reabsorption which is compensated for by pressure natriuresis. Enhanced pressure natriuresis requires persistently elevated blood pressure which leads to hypertension if maintained for many years. The phenomenon of salt sensitivity does not become apparent with a sodium intake of less than 50 mmol/day. Although enhanced noradrenergic sensitivity also persists with this low-sodium intake, salt-sensitive subjects are able to compensate for the enhanced rate of proximal tubular sodium reabsorption by reabsorbing less sodium at the distal tubules as compared with that reabsorbed by salt-resistant subjects. Enhanced noradrenergic sensitivity and enhanced proximal tubular sodium reabsorption, however, cannot be compensated for by fine-tuning aldosterone secretion while on the usual high sodium diet containing greater than 100 mmol/day. Under these conditions aldosterone secretion is already suppressed to its basal rate and cannot be suppressed more in salt-sensitive than in salt-resistant subjects. Therefore with the usual high sodium diet the enhanced rate of proximal tubular sodium reabsorption in salt-sensitive subjects is compensated for by enhanced pressure natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)