Hypertension occurs more commonly in obese than in lean persons at virtuall
y every age. A variety of endocrine, genetic, and metabolic mechanisms have
been linked to the development of obesity hypertension. These include insu
lin resistance and hyperinsulinemia, increased serum aldosterone levels, sa
lt sensitivity and expanded plasma volume in the presence of increased peri
pheral vascular resistance, a genetic predisposition, and possibly increase
d leptin levels. Pressure and volume overload are present in obese hyperten
sives. This leads to a mixed eccentric-concentric form of left ventricular
hypertrophy and increases the predisposition to congestive heart failure. W
eight loss, even in modest decrements, is effective in reducing obesity-hyp
ertension, possibly by ameliorating several of the proposed pathophysiologi
c mechanisms. There are currently no specific recommendations concerning ph
armacotherapy of obesity-hypertension because each drug group has pros and
cons.