ABSTRACT
Blood pressure sensitivity to sodium intake is present in 50 to 60% of patients with hypertension. Epidemiologic studies suggest that there is a variety of pathophysiologic mechanisms leading to sodium-sensitive hypertension. The most recently described group of sodium-sensitive hypertensives are nonmodulators. This group differs from other forms of sodium-sensitive hypertensives in that in a sodium-restricted state, their plasma renin activities are normal or high rather than low. A plausible model providing a mechanistic link between the adrenal and renal abnormalities has been proposed. Given the dominant effect of the renin-angiotensin system on the response to sodium intake in both organs, it has been suggested that primary alterations in the local renin-angiotensin systems could account for the observed abnormalities. The chapter summarizes the features of one such entity — nonmodulators — who comprise a substantial fraction of the essential hypertensive population. They are defined as individuals in whom sodium intake fails to modulate the vascular and adrenal responses to AngII.
