Simulated microgravity enhances vasoconstrictor responsiveness of rat basilar artery.
Simulated microgravity enhances vasoconstrictor responsiveness of rat basilar artery.
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DOI：
10.1152/jappl.2001.90.6.2296
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发表时间：
2001-06
影响因子：
3.3
通讯作者：
Le-Ning Zhang;Li-fan Zhang;Jin Ma
中科院分区：
文献类型：
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作者：
Le-Ning Zhang;Li-fan Zhang;Jin Ma
最近，在模拟微重力后观察到大鼠脑血管肥大和肌源性张力增加。预计模拟微重力也可能诱发脑血管的过度反应。为了检验这一假设，对 Sprague-Dawley 大鼠进行了 4 周的尾部悬挂后肢卸荷 (TS)，以模拟微重力对心血管失调的影响。 4周后，检查TS大鼠分离的基底动脉环对受体介导和非受体介导的血管收缩剂（例如KCl、精氨酸加压素或5-羟色胺（5-HT））和血管扩张剂（例如ACh、凝血酶、腺苷或硝普钠）的血管反应性，并与同时对照（Cn）大鼠的血管反应性进行比较。在本研究的第一部分中，发现TS大鼠的基底动脉环中KCl、精氨酸加压素或5-HT等血管收缩剂引起的最大等长收缩反应性增强，而TS和Cn大鼠对血管舒张剂的血管舒张反应性没有显着差异。本研究的第二部分发现，去除内皮对 TS 大鼠基底动脉环对 5-HT 的收缩反应性没有影响，但显着增强了 Cn 大鼠基底动脉环的反应性，达到与 TS 大鼠相当的程度。应用四乙铵对 TS 基底动脉环中 5-HT 的收缩反应也没有影响，但显着增加了内皮完整的 Cn 大鼠基底动脉环的反应性。这些结果表明，4周模拟微重力增强了基底动脉环对受体和非受体介导的血管收缩剂的血管收缩反应性，并且5-HT诱导的TS大鼠基底动脉收缩的增强是由于内皮依赖性机制的损伤。这些结果表明，内皮衍生的超极化因子是大鼠基底动脉对 5-HT 收缩反应的内皮依赖性减弱调节机制的原因。
Recently, hypertrophy and increased myogenic tone of brain vessels have been observed in rats after simulated microgravity. It is expected that simulated microgravity may also induce hyperreactivity of brain vessels. To test this hypothesis, Sprague-Dawley rats were subjected to a 4-wk tail-suspended hindlimb unloading (TS) to simulate the cardiovascular deconditioning effect of microgravity. After 4 wk, the vasoreactivity of isolated basilar arterial rings from TS rats to both receptor- and non-receptor-mediated vasoconstrictors, such as KCl, arginine vasopressin, or 5-hydroxytryptamine (5-HT), and vasodilators such as ACh, thrombin, adenosine, or sodium nitroprusside were examined and compared with those from simultaneous control (Cn) rats. In the first part of this study, it was found that the maximal isometric contractile responsiveness evoked by vasoconstrictors such as KCl, arginine vasopressin, or 5-HT was enhanced in basilar arterial rings from TS rats, whereas vasodilatory responsiveness to vasodilators showed no significant difference between TS and Cn rats. In the second part of this study, it was found that removal of the endothelium had no effects on the contractile responsiveness to 5-HT in basilar arterial rings from TS rats but enhanced markedly the responsiveness in basilar arterial rings from Cn rats to an extent comparable with that of TS rats. Application of tetraethylammonium also had no effects on the contractile response to 5-HT in basilar arterial rings from TS but significantly increased the responsiveness of basilar arterial rings from Cn rats with endothelium intact. These results showed that 4-wk simulated microgravity enhanced the vascular contractile responsiveness of basilar arterial rings to both receptor- and non-receptor-mediated vasoconstrictors, and the enhancement of 5-HT-induced contraction in TS rat basilar arteries was due to an impairment of endothelium-dependent mechanism. These results suggest that endothelium-derived hyperpolarizing factors are responsible for this endothelium-dependent attenuating modulatory mechanism in contractile responsiveness of rat basilar arteries to 5-HT.