Abstract

AbstractCardiovascular morbidity and mortality is exceedingly high in patients with chronic renal failure. Sympathetic overactivity is an important pathomechanism contributing to progression of renal disease as well as cardiovascular complications. For more than 30 years it has been known that plasma levels of norepinephrine are elevated in chronic renal failure pointing to increased sympathetic nerve activity. The kidneys are richly innervated by efferent sympathetic and afferent sensory nerves. They participate in many reflex adjustments of renal function. Initially, this finding had not been attributed to increased efferent sympathetic drive, but rather to reduced renal clearance and defective neuronal reuptake of norepinephrine.At this time, however, the evidence for increased sympathetic drive is solid. Interventions to reduce sympathetic overactivity will provide new therapeutic approaches. The available experimental and clinical evidence to suggest such a pathophysiological role of sympathetic overactivity is summarized in this current review.

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