Abstract
Interest for the role of the sympathetics in the genesis of hypertension has come full circle from early enthusiasm, through a period of neglect, to present understanding that strong evidence cannot be ignored. Sympathetic overactivity starts in childhood and is easily evident in 30% of patients with incipient hypertension. Later, in advanced hypertension, altered cardiovascular responsiveness obscures the obvious signs of sympathetic overactivity but the brain maintains its decisive pathophysiologic role. The early onset, the bimodal distribution of the neurogenic "hyperkinetic" pattern and familial aggregation suggest a genetic component in sympathetic overactivity. Patients with hypertension are at high risk for coronary disease and some of that risk is not directly related to blood pressure elevation. High sympathetic tone explains the pathophysiology of "pressure-independent" risk for premature coronary atherosclerosis in hypertension and for excess mortality/morbidity in patients who had already developed coronary heart disease.