Sympathetic nervous system: contribution to human hypertension and related cardiovascular diseases

Abstract

Sympathetic nervous system activation has been documented in several cardiovascular disorders. In some, characterized by cardiac failure and portal hypertension accompanying hepatic cirrhosis, the sympathetic nervous stimulation is reflex and, to some extent, compensatory but has adverse consequences. For example, in cardiac failure, the sympathetic nerves of the heart are preferentially stimulated, providing adrenergic support to the failing myocardium but at the probable cost of arrhythmogenesis and progressive myocardial deterioration. The sympathetic activation present in patients with essential hypertension, which involves the sympathetic outflows to skeletal muscle, heart, and kidneys and is seen particularly in younger patients, differs from these examples in that the sympathetic nervous stimulation is apparently not reflex and the primary cause is unknown. There is, however, evidence that activation of forebrain pressor noradrenergic nuclei may be of importance as an underlying central nervous system mechanism. This sympathetic nervous stimulation in patients with essential hypertension, in addition to initiating the blood pressure elevation, may also contribute to the commonly associated metabolic abnormalities of insulin resistance and hyperlipidemia, with neural vasoconstriction having metabolic consequences, impairing glucose delivery and causing insulin resistance in muscle, and retarding postprandial clearing of lipids in liver. Trophic effects of sympathetic activation on cardiovascular growth are claimed but have yet to be demonstrated conclusively in humans.