Woodman Christopher R, Turk James R, Williams Daniel P, Laughlin M Harold
Department of Biomedical Sciences, The Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211, USA.
J Appl Physiol (1985). 2003 May;94(5):2017-26. doi: 10.1152/japplphysiol.01025.2002.
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 N(G)-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 PGI(2)-mediated relaxation. Ex attenuates the effects of HF by enhancing a vasodilator mechanism independent of NO and PGI(2).
运动训练（Ex）通过增强猪肱动脉（Br）中一氧化氮（NO）介导的血管舒张作用，减弱高脂血症对内皮功能的影响。成年雌性猪被喂食正常脂肪（NF）或高脂肪（HF）饮食20周。在开始饮食4周后，猪进行运动训练或保持久坐（Sed）16周。HF损害了对乙酰胆碱（ACh）的舒张反应（P = 0.03）。HF与Sed相结合对ACh诱导的舒张反应的损害比单独的HF或Sed更严重（P = 0.0002）。HF损害了对高剂量缓激肽（BK）的舒张反应（P = 0.0002）。运动训练显著改善了ACh诱导的舒张反应（P = 0.01），并倾向于改善对BK的舒张反应（P = 0.38）。为了确定HF和运动训练影响对ACh和BK舒张反应的机制，在存在N(G)-硝基-L-精氨酸甲酯（L-NAME；抑制一氧化氮合酶）、吲哚美辛（Indo；抑制环氧化酶）或L-NAME + Indo的情况下评估舒张反应。在存在L-NAME、Indo或L-NAME + Indo时，HF和NF动脉之间ACh诱导的舒张反应不再有差异；然而，运动训练组的舒张反应仍高于久坐组动脉。在存在L-NAME或Indo时，BK诱导的舒张反应不再受HF影响，但运动训练可增强该反应。在存在L-NAME + Indo时，BK诱导的舒张反应在HF组和运动训练组均增强。这些数据表明，高脂血症通过损害NO和前列环素（PGI(2)）介导的舒张反应，损害了ACh和BK诱导的舒张反应。运动训练通过增强一种独立于NO和PGI(2)的血管舒张机制，减弱了HF的影响。
