title: The role of obesity in the pathogenesis of hypertension.
abstract: The rapid rise in the incidence and prevalence of obesity and the concomitant increase in the incidence and prevalence of hypertension have fueled investigation into the role of obesity in the pathogenesis of hypertension. The genetic background that predisposes obese individuals to hypertension is being elucidated, and the importance of adipose tissue as an endocrine organ in the pathogenesis of hypertension is increasingly being recognized. Visceral adipose tissue is critical in the production of pathologic cytokines that are thought to mediate obesity-induced hypertension. Changes in the types and levels of adipocytokines that result from the accumulation of aberrant adipose tissue directly leads to alterations in systemic vascular resistance, sodium retention and sympathetic nervous system activity. Key changes in adipocytokine levels seen in obesity-induced hypertension include increased leptin and adiponectin levels. Another important mechanism in obesity-induced hypertension is the generation of angiotensin II and direct stimulation of aldosterone production. The increased sympathetic nervous system activity seen in obesity-associated hypertension leads to increased renal sodium retention and increased systemic vascular resistance. Increased systemic vascular resistance can also occur directly in obese individuals through vascular fibrosis and lipid deposition. Obesity should no longer be simply considered as a marker of cardiovascular risk but should be regarded as an important and primary contributor to the pathophysiology of hypertension.
authors.affiliation: University of Colorado School of Medicine and Denver VA Medical Center, Denver, CO, USA.
authors.forename: Yolanda E
authors.initials: YE
authors.lastname: Bogaert
authors.forename: Stuart
authors.initials: S
authors.lastname: Linas
mesh_terms: D006801:Humans; D006977:Hypertension, Renal / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology*; D009765:Obesity / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology*