Do most antihypertensive agents have a sympatholytic action?

The sympathetic nervous system is a major modulator of cardiovascular functions. Over the past three decades, numerous studies, using various methodologies, have reported the existence of a variety of pre- and postsynaptic sympathetic dysfunctions in essential hypertension. Most of those abnormalities facilitate sympathetic neurotransmission, resulting in a chronic increase in the sympathetic tone and reactivity in an important proportion of hypertensive patients. The chronic sympathetic activation is also associated with major alterations in the balance between postsynaptic adrenergic receptors in cardiovascular tissues. Indeed, an attenuation of beta-adrenergic functions and a potentiation of alpha1-adrenergic functions have been demonstrated in human cardiovascular tissues, suggesting the development of a sympathetic postsynaptic alpha1 dominance during the development and evolution of hypertension. The chronic activation of the sympathetic system is deleterious and could contribute to the development of most cardiovascular complications associated with hypertension. One of the major aims of antihypertensive therapy should be to attenuate pre- or postsynaptic sympathetic tone. Most antihypertensive drugs have been found to improve either pre- or postsynaptic sympathetic functions in hypertensive patients. At the presynaptic level, the effects of antihypertensive drugs have been found to be more variable. At the postsynaptic level, all currently used antihypertensive drugs have been found to attenuate alpha1-adrenergic functions either by interfering directly with intracellular mechanisms underlying alpha1-adrenergic functions or indirectly by decreasing the release of norepinephrine from peripheral sympathetic nerves.