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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; Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA
3 Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada
* To whom correspondence should be addressed. E-mail: laughlinm{at}missouri.edu.
We tested the hypothesis that exercise training (EX) attenuates hypercholesterolemia-induced impairment of endothelium-dependent relaxation (EDR) in male porcine coronary arteries (LAD) by increasing nitric oxide (NO) release (due to increased eNOS expression) and/or increased bio-activity of NO. Adult male pigs were fed a normal fat (NF) or high fat (HF) diet for 20-24 weeks. Pigs were EX or remained sedentary (SED) for 16-20 weeks, beginning after 4 weeks on diet. Four groups of pigs were used: NF-SED, NF-EX, HF-SED, and HF-EX. HF enhanced LAD contractions induced by KCl, aggregating platelets (AP), and serotonin (5-HT). AP and 5-HT produced EDR following blockade of cyclooxygenase with indomethacin (Indo) and smooth muscle 5-HT2 receptors with ketanserin. HF impaired EDR induced by AP, 5-HT, and bradykinin (BK). Results indicate a decreased contribution of NO to EDR in HF-SED LADs, since the % BK-induced EDR inhibited by NG-nitro-L-arginine methyl ester (L-NAME) was 27% in NF-SED and 34 % in NF-EX but only 17 % in HF-SED. Also, L-NAME + Indo results indicate release of an Indo-sensitive vasoconstrictor contributes to blunted EDR in HF-SED LAD. Immunoblot/immunohistochemistry results indicate the following: 1) LAD eNOS protein content was similar among groups., 2) HF decreased LAD superoxide dismutase (SOD) but increased caveolin-1 (CAV-1) content., and 3) EX increased SOD content of HF LADs. We conclude that HF impairs EDR by impairing the contribution NO released from NOS (due to decreased SOD and increased CAV-1 protein content) and by production of an Indo-sensitive vasoconstrictor. EX preserves EDR in HF LADs by decreasing the production of the constrictor and increasing NO-release by NOS and/or NO bioactivity/bioavailability.
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