Adrenergic overactivity is a common hallmark of both essential hypertension and congestive heart failure. Indirect and direct measures of sympathetic function have clearly shown that sympathetic activation characterizes essential hypertension. This adrenergic overactivity appears to be related to the severity of the hypertensive state, being detectable in its early stages and showing a progressive increase with the severity of the disease. Essential hypertension is also associated with an impaired baroreflex control of vagal activity, whereas baroreceptor modulation of sympathetic nerve traffic remains unaltered, although undergoing a resetting phenomenon. In contrast, secondary hypertension is not associated with an increased adrenergic activity, thus suggesting that an enhancement in efferent sympathetic outflow is a peculiar feature of essential hypertension. Congestive heart failure is a condition also characterized by sympathetic activation, whose degree is proportional to the clinical severity of the disease. This is paralleled by an impairment in arterial baroreceptor modulation of both vagal and sympathetic activity, thus suggesting that the adrenergic overactivity in congestive heart failure is triggered by a reduced afferent restraint on the vasomotor centre. Chronic angiotensin-converting enzyme inhibition reduces the degree of both sympathetic activation and baroreflex dysfunction occurring in heart failure patients, a finding which documents that the neurohumoral abnormalities can be at least partially reversed by pharmacologic treatment
