Chen S J, Wu C C, Yen M H
Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan, ROC.
J Biomed Sci. 2001 May-Jun;8(3):248-55. doi: 10.1007/BF02256598.
Exercise training has reversible beneficial effects on cardiovascular diseases, e.g. hypertension, which may result from a decrease in systemic vascular resistance. The purpose of this study was to investigate possible mechanisms associated with the changes in vascular reactivity in large and small arteries with vasoconstrictors and vasodilators in rats after exercise. Wistar-Kyoto rats were trained for 8 weeks (Ex group) on a treadmill and compared with sedentary counterparts (Sed group). After the measurement of blood pressure and heart rate at 8 weeks, rat mesenteric arteries and thoracic aortas were excised and prepared as rings for this study. In addition, special care was taken not to damage the endothelium of the preparations. Our results showed that exercise training for 8 weeks (1) not only prevented an increase in blood pressure but also caused a fall in heart rate, (2) attenuated the contractions induced by both prostaglandin F(2alpha) (PGF(2alpha)) and high K(+) in the mesenteric artery, but reduced the PGF(2alpha)-induced contraction in the aorta only, (3) enhanced the relaxation elicited by acetylcholine (ACh) in both mesenteric arteries and aortas, and (4) increased nitrate [an indicator of nitric oxide (NO) formation] in plasma. The enhancement of ACh-induced relaxation in the mesenteric arteries in the Ex group was suppressed by pretreatment with N(omega) -nitro-L-arginine methyl ester (L-NAME), tetraethylammonium (TEA; a nonselective inhibitor of K(+) channels) or charybdotoxin [CTX; a selective inhibitor of large-conductance calcium-activated K(+) (BK(Ca)) channels], whereas in the aorta that response was attenuated by TEA or CTX and almost completely abolished by L-NAME. However, with a combination of L-NAME plus CTX in the mesenteric artery, ACh-induced relaxation was completely abolished in the Sed group, but not in the Ex group. These results suggest that in addition to NO, activation of BK(Ca) channels in the vascular beds, at least in part, also contributes to vasodilatation in animals with exercise training.
运动训练对心血管疾病，如高血压，具有可逆的有益影响，高血压可能是由全身血管阻力降低引起的。本研究的目的是探讨运动后大鼠大小动脉血管对血管收缩剂和血管舒张剂反应性变化的可能机制。将Wistar-Kyoto大鼠在跑步机上训练8周（运动组），并与久坐不动的对照组（对照组）进行比较。在8周时测量血压和心率后，切除大鼠肠系膜动脉和胸主动脉并制备成环用于本研究。此外，特别注意不损伤标本的内皮。我们的结果表明，8周的运动训练（1）不仅防止了血压升高，还导致心率下降，（2）减弱了前列腺素F(2α)（PGF(2α)）和高钾在肠系膜动脉中诱导的收缩，但仅降低了主动脉中PGF(2α)诱导的收缩，（3）增强了乙酰胆碱（ACh）在肠系膜动脉和主动脉中引起的舒张，（4）增加了血浆中硝酸盐[一氧化氮（NO）生成的指标]。运动组肠系膜动脉中ACh诱导的舒张增强被N(ω)-硝基-L-精氨酸甲酯（L-NAME）、四乙铵（TEA；钾通道的非选择性抑制剂）或蝎毒素[CTX；大电导钙激活钾（BK(Ca)）通道的选择性抑制剂]预处理所抑制，而在主动脉中，该反应被TEA或CTX减弱，几乎被L-NAME完全消除。然而，在肠系膜动脉中联合使用L-NAME和CTX时，ACh诱导的舒张在对照组中完全被消除，但在运动组中没有。这些结果表明，除了NO外，血管床中BK(Ca)通道的激活至少部分也有助于运动训练动物的血管舒张。
