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Department of Physiology, National Cheng-Kung University Medical College, Tainan, Taiwan 701, Republic of China
Chronic exercise enhances endothelium-dependent vasodilating responses. To investigate whether this is due to a change in endothelial Ca2+ signaling, we examined intracellular Ca2+ concentration ([Ca2+]i) level in rat aortic endothelium in response to acetylcholine (ACh) or ATP. Four-week-old male Wistar rats were divided into control and exercise groups. The exercised animals ran on a treadmill at a moderate intensity for 60 min/day, 5 day/wk, for 10 wk. Rat aortas were then excised and loaded with fura 2. After the aortas were mounted on a flow chamber, these specimens were observed under an epifluorescence microscope equipped with ratio-imaging capability. Our results showed that 1) chronic exercise increased both ACh- and ATP-induced [Ca2+]i responses; 2) ACh induced heterogeneous [Ca2+]i elevation in individual endothelial cells; and 3) the exercise effect on ACh-evoked endothelial [Ca2+]i elevation was inhibited by the Ca2+ influx blocker SKF-96365, by a Ca2+-free buffer, or by high concentrations of extracellular K+. We conclude that chronic exercise increases ACh-induced [Ca2+]i elevation in rat aortic endothelium in situ, possibly by facilitating Ca2+ influx.
exercise training; acetylcholine; intracellular calcium; aortic endothelium
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