Essential hypertension has long been assumed to be a multifactorial disease. However, recent evidence suggests that it is a syndrome rather than a disease with a common symptom–an elevated blood pressure. One large segment of the hypertensive population–approximately 60%–has in common an increased blood pressure sensitivity to salt intake. Further analysis of this subgroup suggests that it is also heterogeneous, consisting of at least six major entities: renal parenchymal disease, bilateral renal artery stenosis, primary aldosteronism, acromegaly, low renin essential hypertension, and the most recently described entity–nonmodulating essential hypertension. This subset's name is derived from the fact that sodium intake does not modify (modulate) renovascular and adrenal responses to angiotensin II, as occurs in normotensives and modulating hypertensive patients. The following abnormalities have been reported in these patients: (1) a failure of renal blood flow to increase with salt loading; (2) a reduced ability to excrete a salt load; (3) reduced renin suppression both by salt and angiotensin II; and (4) a hypertensive response to salt load. These patients also have a strong family history for hypertension and an increase in erythrocyte sodium countertransport. With a better understanding of the mechanisms underlying the elevated blood pressure in a specific patient, a more rational approach to therapy is possible. For example, in the salt-sensitive hypertensive patient a diuretic would be the presumed treatment of choice. While this is correct for some salt-sensitive hypertensives, in nonmodulators diuretics may be relative ineffective while converting enzyme inhibitors may be more effective because they specifically correct the underlying pathophysiologic derangement.