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1 Physiology, Medical College of Georgia, Augusta, GA, USA
* To whom correspondence should be addressed. E-mail: dstepp{at}mcg.edu.
Obesity causes whole body insulin resistance and impaired vasodilation to nitric oxide. Because nitric oxide is a major contributor to the regulation of mesenteric blood flow, the mesenteric circulation of obese animals is faced with reduced capacity to increase flow and increased demand for flow associated with elevated consumption of food. This study hypothesized that insulin-resistance impairs NO-mediated dilation but that constrictor reactivity would be reduced to compensate in obese animals. We further hypothesized that elevated super-oxide levels caused impaired responses to NO in insulin resistance. Vasodilator and vasoconstrictor reactivity of mesenteric resistance arteries from Lean (LZR) and Obese (OZR) Zucker rats were examined in vitro using videomicroscopy. Insulin resistance independent of obesity was induced via fructose feeding in LZR (FF-LZR). Endothelium-dependent NO-mediated dilation was reduced in OZR and FF-LZR compared to LZR. Impairments in NO-mediated dilation were reversed with 1mM tempol, an SOD-mimetic. Constrictor reactivity to norepinephrine was reduced in OZR but not FF-LZR relative to LZR. Basal mesenteric vascular resistance (MVR) was similar in LZR and OZR, despite impaired NO-dependent dilation in OZR. MVR was increased in FF-LZR relative to LZR. These data indicate that there is reduced constrictor reactivity in OZR that may offset the impaired NO-mediated dilation and preserve mesenteric blood flow in hyperphagic, obese animals.
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