运动训练对雄性大鼠肠系膜动脉床对去氧肾上腺素和氯化钾反应性的影响。

Effects of exercise training on responsiveness of the mesenteric arterial bed to phenylephrine and KCl in male rats.

作者信息

Jansakul C, Hirunpan P

机构信息

Department of Physiology, Faculty of Science, Prince of Songkla University, Hat-Yai, Thailand 90112, USA.

出版信息

Br J Pharmacol. 1999 Aug;127(7):1559-66. doi: 10.1038/sj.bjp.0702697.

DOI:10.1038/sj.bjp.0702697

PMID:10455310

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1566144/

Abstract

We aimed to determine whether there are any changes in responsiveness of the mesenteric arterial beds to phenylephrine (Phe) and KCl in exercise-trained rats, and whether vascular endothelium and/or vascular smooth muscle play a role in these changes. 2. Adult male rats were subjected to a swimming schedule every day for 28-33 days. Studies were performed in vitro using Krebs perfused mesenteric arterial beds. 3. Maximum perfusion pressure responses to KCl and Phe of the mesenteric arterial beds from exercise-trained rats were significantly lower than those from sedentary controls. However, these differences disappeared after blocking the nitric oxide synthase by NG-nitro-L-arginine (L-NOARG). 4. 3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulphonate (CHAPS, 3 mg ml(-1), 2 min infusion) caused a significant increase in maximum perfusion pressure responses to KCl to the same extent in both exercise-trained and sedentary control rats. CHAPS caused about a 4.5 fold leftward shift of the curve with no change in maximum response to Phe for the mesenteric arterial beds from sedentary control rats, but not for those obtained from exercise-trained rats. However, these differences were abolished in the presence of L-NOARG. 5. Indomethacin did not alter the dose-response curves to KCl or Phe in either swimming or control groups. 6. These results suggest that there was a lower vascular responsiveness to KCl and Phe in exercise-trained rats at rest. The decrease in reactivities to KCl or decrease in sensitivity to Phe after having endothelium impairment by CHAPS of the mesenteric arterial beds of exercise-trained rats were due to an increase in both spontaneous release and upregulation of phenylephrine-stimulated release of nitric oxide from both the vascular endothelium and the vascular smooth muscle cells, and may not be a consequence of an increase in vasodilator prostaglandins by the vascular bed.

摘要

我们旨在确定运动训练大鼠肠系膜动脉床对去氧肾上腺素（Phe）和氯化钾（KKKCl）的反应性是否有任何变化，以及血管内皮和/或血管平滑肌在这些变化中是否起作用。2. 成年雄性大鼠每天进行游泳训练，持续28 - 33天。使用Krebs灌注的肠系膜动脉床进行体外研究。3. 运动训练大鼠肠系膜动脉床对KCl和Phe的最大灌注压反应显著低于久坐不动的对照组。然而，用NG - 硝基 - L - 精氨酸（L - NOARG）阻断一氧化氮合酶后，这些差异消失。4. 3 - [(3 - 胆酰胺丙基)-二甲基铵]-1 - 丙烷磺酸盐（CHAPS，3 mg/ml，输注2分钟）使运动训练大鼠和久坐不动的对照大鼠对KCl的最大灌注压反应均显著增加到相同程度。CHAPS使久坐不动的对照大鼠肠系膜动脉床对Phe的曲线向左移动约4.5倍，最大反应无变化，但运动训练大鼠的肠系膜动脉床对Phe的最大反应无此变化。然而，在L - NOARG存在的情况下，这些差异消失。5. 吲哚美辛在游泳组或对照组中均未改变对KCl或Phe的剂量反应曲线。6. 这些结果表明，运动训练大鼠在静息状态下对KCl和Phe的血管反应性较低。运动训练大鼠肠系膜动脉床经CHAPS损伤内皮后，对KCl反应性降低或对Phe敏感性降低，是由于血管内皮和血管平滑肌细胞中一氧化氮的自发释放增加以及去氧肾上腺素刺激释放上调所致，可能不是血管床中血管舒张前列腺素增加的结果。