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1 Department of Biomedical Sciences, University of Missouri, Columbia, MO, USA
2 Department of Biomedical Sciences, University of Missouri, Columbia, MO, USA; Department of Veterinary Pathobiology, University of Missouri, Columbia, MO, USA
3 Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada
4 Department of Biomedical Sciences, University of Missouri, Columbia, MO, USA; Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO, USA; Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA
* To whom correspondence should be addressed. E-mail: laughlinm{at}missouri.edu.
Hypercholesterolemia is reported to attenuate endothelial function and exercise training has been reported to augment endothelial function. We hypothesized that exercise training would improve endothelial function of coronary arterioles from pigs in the early stages of cardiovascular disease induced by a high fat/cholesterol diet. Yucatan miniature swine were fed a normal (NF) or high fat (HF, 2% cholesterol) diet for 20wks in which 8% and 46% of their kcal were derived from fat, respectively. Both groups were subdivided into sedentary (SED) or exercise trained (EX) groups. This resulted in four experimental groups: NFSED, NFEX, HFSED and HFEX. Endothelial function was assessed in coronary arterioles 75-100µm in diameter dissected from the left ventricular apex. Responses to endothelial dependent dilation induced by bradykinin (BK), ADP and flow were similar in all four groups while dilation to aggregating platelets in the presence of indomethacin and Ketanserin was attenuated in HFSED arterioles (p = 0.01). The attenuated response to aggregating platelets was prevented/reversed in HFEX arterioles (p = 0.03). In HFSED arterioles, BK induced release of an indomethacin sensitive prostanoid constrictor. In contrast, after exercise training there was no evidence of this constrictor and BK induced release of an indomethacin sensitive prostanoid dilator in HFEX arterioles (p = 0.04). eNOS protein in arterioles was significantly reduced by HF (p < 0.05) and increased by EX (p < 0.05). Interestingly, the relative contribution of nitric oxide to BK induced dilation, as assessed with L-NAME, was similar in NF, HF, SED and EX arterioles. These results suggest that in the early stages of cardiovascular disease, a high fat/cholesterol diet has modest effects on endothelial dependent dilation in coronary arterioles; nonetheless these effects are prevented/reversed with exercise training.
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