Obesity, a major health problem in industrialized societies, is associ
ated with a high incidence of cardiovascular complications such as hyp
ertension, ischemic heart disease and stroke. However, the underlying
mechanism relating obesity and these cardiovascular events is not clea
r. In lean subjects even slight elevations in plasma insulin concentra
tion exert marked effects on the cardiovascular system, and these effe
cts are directly related to insulin (rather than to insulin-induced st
imulation of intermediary metabolism). Moreover, insulin's vascular ef
fects are mediated both by the sympathetic nervous system and the L-ar
ginine nitric oxide pathway. Obesity is characterized by sustained sym
pathetic activation (possibly related to chronic hyperinsulinemia) and
an impaired vasodilator responsiveness to insulin. Although, undoubte
dly many factors contribute to the increased incidence of cardiovascul
ar complications in overweight subjects, sympathetic activation could
be one important mechanism and either trigger acute events or-possibly
in conjunction with an impairment in insulin-induced vasodilation-con
tribute to sustained elevation of arterial pressure.