Endothelial dysfunction, increased sympathetic activity, renin-angiotensin overactivation, and insulin resistance are proposed as primary mechanisms mediating obesity-associated hypertension.
Understanding the mechanisms of endothelial dysfunction and metabolic regulation in obesity is crucial for developing targeted therapies for obesity-associated hypertension.
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.
Lobato et al. (Sun,) conducted a review in Obesity-associated hypertension. Endothelial dysfunction, increased sympathetic activity, renin-angiotensin overactivation, and insulin resistance are proposed as primary mechanisms mediating obesity-associated hypertension.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: