Several studies have demonstrated that essential hypertension is accompanie
d by sympathetic activation, which contributes to blood pressure elevation.
Sympathetic activation also has adverse consequences in hypertensive patie
nts beyond initiating blood pressure elevation. There is evidence that neur
al vasoconstriction has metabolic effects in skeletal muscle, impairing glu
cose delivery to muscles. In the liver, retarding of post prandial clearanc
e of lipids contributes to hyperlipidemia. Cardiac sympathetic activation i
s a probable cause of sudden death in hearth failure. A trophic effect of s
ympathetic activation on cardiovascular growth is also likely, contributing
to the development of left ventricular hypertrophy. Consequently, one of t
he major aims of antihypertensive therapy should be to attenuate sympatheti
c tone.
It is possible that, among the antihypertensive drugs available, those inhi
biting the sympathetic nervous system might best reduce cardiovascular risk
.