1. The volume of work reporting insulin resistance in multiple forms o
f chronic hypertension has generated tremendous interest in whether th
is abnormality is an important factor in causing hypertension, Insulin
resistance, however, is an imprecise term used interchangeably to des
cribe widely disparate types of impairment in insulin action throughou
t the body and the type of insulin resistance has major ramifications
regarding its potential for inducing long-term increases in blood pres
sure (BP). 2. Hepatic insulin resistance (impaired insulin-mediated su
ppression of hepatic glucose output) is the primary cause of fasting h
yperinsulinaemia and is a cardinal feature of obesity hypertension. Ev
idence from chronic insulin infusion studies in rats suggests hyperins
ulinaemia can increase BP under some conditions; however, conflicting
evidence in humans and dogs leaves in question whether hyperinsulinaem
ia is a factor in hypertension induced by obesity. 3. Peripheral insul
in resistance (impaired insulin-mediated glucose uptake, primarily of
an acute glucose load in skeletal muscle) also present in obesity hype
rtension, but now reported in lean essential hypertension as well, is
linked most notably to impaired insulin-mediated skeletal muscle vasod
ilation. This derangement has also been proposed as a mechanism throug
h which insulin resistance can cause hypertension. 4. The present revi
ew will discuss the lack of experimental or theoretical support for th
at hypothesis and will suggest that a direct link between insulin resi
stance and BP control map not be the best way to envision a role for i
nsulin resistance in cardiovascular morbidity and mortality.