An increasing number of clinical trials have demonstrated that obese patients are more likely than lean individuals to be hypertensive. Moreover, both obesity and arterial hypertension have been identified as independent risk factors for cardiovascular disease. Pathophysiologically, obesity appears to have a major influence on the hemodynamic changes associated with hypertension. The available evidence suggests that at any given level of arterial pressure, obese hypertensive patients have a higher cardiac output and lower total peripheral resistance than do lean patients. Recent reports have indicated that obesity exerts a disparate effect on target organs in hypertension. Whereas at rest obesity seems to mitigate cardiovascular changes in the systemic vascular bed caused by hypertension, no such mitigation was observed in the renovasculature; left ventricular hypertrophy as a major cardiovascular risk factor was even exacerbated by the presence of obesity. The different hemodynamic patterns in obese hypertensive patients have recently been shown clinically relevant for treating hypertensive patients.