Sympathetic activation in the pathogenesis of hypertension and progressionof organ damage

Although animal models of hypertension have clearly shown that high blood p ressure is associated with and is probably caused by an increase in sympath etic cardiovascular influences, a similar demonstration in humans has been more difficult to obtain for methodological reasons. There is, now evidence , however, of increased sympathetic activity in essential hypertension. Thi s article will review this evidence by examining data showing that plasma n orepinephrine is increased in essential hypertension and that this is also the case for systemic and regional norepinephrine spillover, as well as for the sympathetic nerve firing rate in the skeletal muscle nerve district. E vidence will also be provided that sympathetic activation is a peculiar fea ture of essential hypertension, particularly in its early stages, with seco ndary forms of high blood pressure not usually characterized by an increase d central sympathetic outflow, Humoral, metabolic, reflex, and central mech anisms are likely to be the factors responsible thr the adrenergic activati on characterizing hypertension, which may also promote the development and progression of the cardiac and vascular alterations that lend to hypertensi on-related morbidity and mortality, independent of blood pressure values. T his represents the rationale for considering sympathetic deactivation one o f the major goals of antihypertensive treatment.