Abstract
Hypertension is a public health challenge of increasing importance because of its high frequency and concomitant risk of cardiovascular and renal disease. It has been estimated that the worldwide prevalence of hypertension was 972 million in 2000, and this number will increase by 60% by the year 2025.1 A large body of evidence indicates that the increasing prevalence of hypertension is sustained by the escalation of overweight and obesity. Actually, most hypertensive patients are also overweight or obese,2 and this may contribute to further deteriorate their cardiovascular risk profile. Similar to hypertension, obesity is independently associated with numerous adverse cardiovascular outcomes, and, most importantly, adipose tissue expansion and hypertension have a synergistic negative impact on cardiovascular prognosis. Hence, the hypertension–obesity pandemic imposes today a considerable burden on societies and healthcare systems that one can reasonably expect to increase further in the next years. The importance of preventing hypertension underscores the critical role of a better understanding of the most common mechanisms underlying its development. The association between obesity and hypertension has been recognized for many decades,2 and an almost linear relation appears between body mass index and systolic and diastolic blood pressures, at least over a body mass index range from 16 to 31 kg/m2.3 Also, risk estimates from the Framingham Heart Study suggest that ≈78% of the hypertension cases in men and 65% in women can be directly attributed to obesity.4 Further evidence for a consistent link between adiposity and hypertension comes from studies showing that weight gain is almost invariably associated with an increase in blood pressure. The increase in blood pressure is closely related to the magnitude of weight gain, and even moderate weight gain is associated with an increased risk of developing hypertension.5 In addition, even modest weight …
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