A significant association between hypertension and obesity has been noted in several epidemiological studies. In particular, a progressive increase has been demonstrated, both in men and women, in the prevalence of hypertension in relation to the different measures of obesity. Such association is independent of age, gender, and also probably the ethnic group. It has also been shown that obesity may antedate and predict the development of hypertension. Even among subjects with normal or optimal blood pressure, the obese subjects are more likely to develop high blood pressure levels in the following years. The opposite can also be true. Hypertensive subjects are more likely to develop obesity than normotensive ones. It has been suggested that initial sympathetic hyperactivity may lead to high blood pressure and progressive hyperstimulation, followed by down-regulation, of beta-adrenergic receptors, with subsequent development of obesity because of the lesser beta-adrenoceptor that induces dissipation of calories. Visceral obesity seems to be more important than subcutaneous obesity with respect to high blood pressure. Finally, in addition to the well established relation between low weight at birth and adult hypertension, it has also been shown that any transient increases in body weight may be paralleled by increases in blood pressure at any time in life. Obesity may be associated with hypertension through an increased sympathetic tone, increased fluid retention and insulin resistance. Animal models of hypertension associated with obesity may be suitable to investigate in detail the pathophysiological mechanisms of such association. In this setting decreased nitric oxide production and resistance to leptin have been identified as important determinants of obesity in hypertension. From a therapeutic standpoint, it is well known that weight reduction is associated with a drop in blood pressure. Unfortunately, however, obese hypertensive subjects who loose weight in the short term often do not succeed to maintain the weight loss, with consequent new gain in body weight and blood pressure. Thus, weight reduction should be maintained in the long term to elicit a sustained and effective antihypertensive efficacy.