A large proportion of hypertensive men and women in Europe and North America are overweight. In obesity, the expanded blood volume increases cardiopulmonary volume, cardiac filling, left ventricular preload, stroke volume and, thereby, left ventricular work. Given enough exposure time, it is probable that all obese persons in the Western hemisphere would become hypertensive unless they succumb to competing causes of death. A postulated causal role of obesity in hypertension is based on epidemiological observations. In prospective studies weight gainers in adolescence are more often hypertensive than weight stable individuals. In the lower socio-economic strata of industrialized countries there is a higher prevalence of obesity and hypertension. Persons with high body weight show the greatest rise of BP with age. More relevant demonstration of a causal relationship is weight reduction in hypertensive patients. The evidence from a variety of sources, a) risk factor reduction and enhanced BP reduction in the Hypertension Detection and Follow-up Program patients on antihypertensive medication who experienced modest weight loss, b) clinical observations of formerly obese hypertensives who can forego BP lowering drugs, and c) the reversibility of haemodynamic change found in many overweight hypertensive patients after losing 10 kg, strongly suggests that the impact of obesity on hypertension is considerable.