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Endurance exercise training improves endothelium-dependent relaxation in brachial arteries from hypercholesterolemic male pigs

Department of Biomedical Sciences, University of Missouri, Columbia, Missouri

Submitted 16 March 2005 ; accepted in final form 17 June 2005

We tested the hypothesis that exercise (Ex) training attenuates hypercholesterolemia-induced impairment of endothelium-dependent relaxation (EDR) in brachial (Br) arteries of adult male pigs by enhancing nitric oxide (NO)-mediated EDR. Adult male pigs were fed a normal-fat (NF) or high-fat/cholesterol (HF) diet for 20 wk. Four weeks after the diet was initiated, pigs were trained or remained sedentary (Sed) for 16 wk, yielding four groups: 1) NF-Sed, 2) NF-Ex, 3) HF-Sed, and 4) HF-Ex. EDR of Br artery rings was assessed in vitro with acetylcholine (ACh) and bradykinin (BK). ACh- and BK-induced relaxation was not impaired by HF; however, relaxation responses were enhanced by Ex in NF and HF arteries. To determine the mechanism(s) by which Ex improved EDR, ACh- and BK-induced relaxation was assessed in the presence of N^G-nitro-L-arginine methyl ester (L-NAME; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), or L-NAME + Indo. ACh- and BK-induced relaxation was inhibited by L-NAME, and L-NAME + Indo, in all groups of arteries. Indo did not inhibit ACh-induced relaxation in any group but did inhibit BK-induced relaxation in HF-Ex arteries. In the presence of L-NAME or L-NAME + Indo, ACh- and BK-induced relaxation in HF-Ex arteries remained greater than in HF-Sed arteries. However, in the presence of Indo, ACh-induced relaxation in HF-Ex arteries was no longer greater than in HF-Sed arteries. These results indicate that EDR is not impaired by hypercholesterolemia in Br arteries from adult male pigs; however, Ex improves EDR in HF Br arteries by enhancing production of endothelium-derived hyperpolarizing factor and/or prostacyclin.

nitric oxide; prostacyclin; endothelium-derived hyperpolarizing factor; endothelial nitric oxide synthase; vascular smooth muscle

This article has been cited by other articles:

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