Abstract
Obesity is strongly associated with high blood pressure, dyslipidemia, and type 2 diabetes. These conditions synergistically increase the risk of cardiovascular events. A number of central and peripheral abnormalities can explain the development or maintenance of high blood pressure in obesity. Of great interest is endothelial dysfunction, considered to be a primary risk factor in the development of hypertension. Additional mechanisms also related to endothelial dysfunction have been proposed to mediate the development of hypertension in obese individuals. These include: increase in both peripheral vasoconstriction and renal tubular sodium reabsorption, increased sympathetic activity and overactivation of both the renin-angiotensin system and the endocannabinoid system and insulin resistance. The discovery of new mechanisms regulating metabolic and vascular function and a better understanding of how vascular function can be influenced by these systems would facilitate the development of new therapies for treatment of obesity-associated hypertension.
Highlights
Obesity is a major worldwide public health problem [1,2], especially in the United States, where approximately 300,000 deaths each year have been attributed to overweight or obesity
Obesity on endothelial function in the microvasculature is the mechanisms linking obesity with endothe- attributable to the reduced nitric oxide (NO) bioavailability as a conlial dysfunction have not yet been fully clarified, several sequence of uncoupled Endothelial nitric oxide synthase (eNOS) [21]. These findings indicate factors have been proposed to mediate this process
Visceral adiposity and/or perivascular adipose tissue dysfunction are directly involved in NO/ endothelium-derived contractile factors (EDCFs) imbalance by promoting a chronic inflammatory state
Summary
Obesity is a major worldwide public health problem [1,2], especially in the United States, where approximately 300,000 deaths each year have been attributed to overweight or obesity. Insulin is essential for normal tissue development, maintaining glucose homeostasis and regulating carbohydrate, lipid, and protein metabolism [37] This hormone has important vascular actions, which include the stimulation of endothelium-dependent NO release, leading to vasodilatation and increased blood flow, favoring glucose uptake by skeletal muscle. It was demonstrated that the effect of vasodilating agents on endothelial cells depends on a direct facilitator action of insulin and that in insulin-deficient states, early alterations of the effects of insulin on endothelial cells might contribute to the impaired reactivity of the microveswww.bjournal.com.br sels [40] Consistent with these results are the observations that treatment with either insulin [20] or the insulin sensitizer metformin [41] corrects the reduced endothelium-dependent vasodilatation without fully improving the metabolic parameters of experimental models of diabetes. It is unclear whether the sympathetic nervous system and endothelial systems are negatively affecting one another, or whether both systems are affected as a consequence of obesity and hypertension
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