English

Abstract

Metabolic and humoral mechanisms have been known to be involved in the development and progression of cardiovascular-related sympathetic overdrive. Sympathetic overactivity in the genesis of major complications of cardiovascular system and associated organ damages has been reported as one of the major participant. Evidences has been provided that sympathetic neural mechanisms may participate in the development of cardiovascular -related target organ damage, such as left ventricular hypertrophy, diastolic dysfunction, impaired arterial compliance vascular atherosclerosis and renal failure. Renalase, a circulating FAD-dependent amine oxidase, has been reported as a secretion in blood form the kidney as well as from heart, skeletal muscle and small intestine and known to alter systemic blood pressure, cardiac & renal function in health and diseases. It has been identified in two isoforms of the human protein and is produced by alternative splicing. In vitro studies have demonstrated that Renalase triggers the release as well as degrades catecholamines such as dopamine, norepinephrine and epinephrine and thus has been claimed to have casual link between sympathetic overdrive and increase risk of cardiovascular dysfunction & related organ damage. This paper discussed the main features of physiological functions of renalase, including its sources of secretion, expression and circulating level and their relevance with adrenergic function in cardiovascular dysfunctions & related organ damage. The paper also reviewed the potential role of renalase in the diagnostic and /or therapeutic approach to cardiovascular disorders & renal diseases, aimed at regulation of sympathetic deactivation.