Obesity and hypertension: from pathophysiology to treatment

While the prevalence of hypertension is clearly increased among the overwei ght persons, the pathophysiological mechanisms underlying this frequent ass ociation of obesity and hypertension are still poorly understood. The expan sion of extracellular volume, inducing hypervolaemia and increased cardiac output, represents the characteristic haemodynamic feature of the obesity-r elated hypertension. The maintenance of hypervolemia in the face of elevate d blood pressure, indicates a resetting of presser natriuresis toward highe r blood pressure. The development of hypertension also indicates an increas e in peripheral vascular resistance, thus the lack of physiological adaptat ion of peripheral resistance to increased cardiac output. The mechanisms un derlying these changes in renal function and vascular reactivity can no lon ger be attributed to hyperinsulinaemia as such, but might be related to ins ulin resistance responsible for the enhancement in presser activity of nora drenaline and angiotensin II. This increased reactivity to presser factors may be due to an inadequate nitric oxide generation by vascular endothelium and to increased sodium and calcium concentration in vascular smooth muscl e cells. The role of increased neuropeptide Y (NPY) activity, may also be i nvolved. As to enhancement of tubular sodium reabsorption, it could be rela ted to histological changes within the renal medulla, leading to compressio n of tubules and vase recta, hence a more efficient sodium reabsorption. As to the therapeutic approach, the low-energy sodium-restricted diet associa ted with increased physical activity, represents the cornerstones of treatm ent for the obesity-related hypertension. If this approach fails, the pharm acological treatment becomes necessary, and the use of the converting enzym e inhibitors seems to be the most appropriate choice of drug therapy for hy pertensive obese patients.