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J Appl Physiol 94: 2017-2026, 2003; doi:10.1152/japplphysiol.01025.2002
8750-7587/03 $5.00
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Vol. 94, Issue 5, 2017-2026, May 2003

Exercise training preserves endothelium-dependent relaxation in brachial arteries from hyperlipidemic pigs

Christopher R. Woodman, James R. Turk, Daniel P. Williams, and M. Harold Laughlin

Department of Biomedical Sciences, and The Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211; and Department of Exercise and Sport Science, College of Health, The University of Utah, Salt Lake City, Utah 84112

We tested the hypothesis that exercise training (Ex) attenuates the effects of hyperlipidemia on endothelial function by enhancing NO-mediated vasorelaxation in porcine brachial (Br) arteries. Adult female pigs were fed a normal-fat (NF) or high-fat (HF) diet for 20 wk. Four weeks after initiation of the diet, pigs underwent Ex or remained sedentary (Sed) for 16 wk. Relaxation to ACh was impaired by HF (P = 0.03). The combination of HF and Sed impaired ACh-induced relaxation more than HF or Sed alone (P = 0.0002). Relaxation to high doses of bradykinin (BK) was impaired by HF (P = 0.0002). Ex significantly improved ACh-induced relaxation (P = 0.01) and tended to improve relaxation to BK (P = 0.38). To determine the mechanism(s) by which HF and Ex affected relaxation to ACh and BK, relaxation was assessed in the presence of NG-nitro-L-arginine methyl ester (L-NAME; to inhibit NO synthase), indomethacin (Indo; to inhibit cyclooxygenase), or L-NAME + Indo. In the presence of L-NAME, Indo, or L-NAME + Indo, ACh-induced relaxation was no longer different between HF and NF arteries; however, relaxation remained greater in Ex than in Sed arteries. In the presence of L-NAME or Indo, BK-induced relaxation was no longer altered by HF but was enhanced by Ex. In the presence of L-NAME + Indo, BK-induced relaxation was enhanced by HF and Ex. These data indicate that hyperlipidemia impairs ACh- and BK-induced relaxation by impairing NO- and PGI2-mediated relaxation. Ex attenuates the effects of HF by enhancing a vasodilator mechanism independent of NO and PGI2.

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


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