Is insulin resistance linked to hypertension?
1. The volume of work reporting insulin resistance in multiple forms of chronic hypertension has generated tremendous interest in whether this abnormality is an important factor in causing hypertension. Insulin resistance, however, is an imprecise term used interchangeably to describe widely disparate types of impairment in insulin action throughout the body and the type of insulin resistance has major ramifications regarding its potential for inducing long-term increases in blood pressure (BP). 2. Hepatic insulin resistance (impaired insulin-mediated suppression of hepatic glucose output) is the primary cause of fasting hyperinsulinaemia and is a cardinal feature of obesity hypertension. Evidence from chronic insulin infusion studies in rats suggests hyperinsulinaemia can increase BP under some conditions; however, conflicting evidence in humans and dogs leaves in question whether hyperinsulinaemia is a factor in hypertension induced by obesity. 3. Peripheral insulin resistance (impaired insulin-mediated glucose uptake, primarily of an acute glucose load in skeletal muscle) also present in obesity hypertension, but now reported in lean essential hypertension as well, is linked most notably to impaired insulin-mediated skeletal muscle vasodilation. This derangement has also been proposed as a mechanism through which insulin resistance can cause hypertension. 4. The present review will discuss the lack of experimental or theoretical support for that hypothesis and will suggest that a direct link between insulin resistance and BP control may not be the best way to envision a role for insulin resistance in cardiovascular morbidity and mortality.
Brands
M W
MW
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216, USA. brands@fiona.umsmed.edu
Hall
J E
JE
Keen
H L
HL
D000818:Animals; D006801:Humans; D006946:Hyperinsulinism / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology*