Insulin has well known metabolic effects. However, depending on the ma
gnitude and duration of the insulin stimulus, this hormone can also pr
oduce vasodilation and vascular smooth muscle growth. The association
of hyperinsulinemia with the metabolic disorders of obesity and non-in
sulin-dependent diabetes, as well as with the cardiovascular pathologi
es of hypertension and atherosclerosis, has led to suggestions that pe
rhaps elevated insulin levels are causally related to these diseases.
Alternatively, insulin resistance may develop following an increase in
skeletal muscle vascular resistance, with or without hypertension, su
ch that a reduction in skeletal muscle bloodflow leads to an attenuate
d glucose delivery and uptake. These hypotheses ar-e explored in this
review by examining the effects of insulin on vascular smooth muscle t
issue during both acute and prolonged exposure. An inter-action among
hyperinsulinemia, hyperglycemia, and hyperlipidemia associated with th
e insulin resistant state is described whereby insulin resistance can
be both a cause and a result of elevated vascular resistance. The asso
ciation between blood flow and insulin stimulated glucose uptake sugge
sts that therapeutic intervention against the development of skeletal
muscle vascular resistance should occur early in individuals genetical
ly predisposed to cardiovascular pathology in order to attenuate, ol a
void, insulin resistance and its sequelae.