| Abstract: The mechanism of postflight cardiovascular deconditioning has been considered as an important problem in the field of gravitational physiology that merits paying great attention to. The recent observations during spaceflight have suggested that adaptive alterations in the arterial vasculature may play a pivotal role in the occurrence of postflight cardiovascular deconditioning. Previous findings from our laboratory have demonstrated that simulated microgravity may result in atrophic change and depressed vasoconstrictor responsiveness in hindquarter vessels, and hypertrophic change in cerebral arteries. However, the vasoreactivity of cerebral arteries is still not known. In the first part of the present work the changes of the vasoreactivity of cerebral arteries were investigated. According to recent advances in the biomedicine of vessels, we have postulated that the tissue renin-angiotensin system (RAS) of the vessels may play an important role in the occurrence of the differentiated vascular adaptation during microgravity. Therefore, in the second part of the present work the alterations of angiotensin receptors were investigated for understanding the mechanism ofvascular adaptational alterations. Whether gravity-based countermeasures should be adopted in the future exploration-class spaceflights in this new century is an urgent science problem that needs further clarification. Hence, in the third part of the present work, the head-up tilt (HUT), standing (STD) and centrifugation were used to simulate the intermittent artificial gravity (IAG), and the preventing effects of them on the structural and functional alterations in cerebral arteries caused by simulated microgravity were investigated.The major findings of the present work are as follows:1. After four weeks of simulated microgravity, the maximal isometric contractile responsiveness of basilar arterial rings evoked by vasoconstrictors, like KC1, AVP or 5-HT was enhanced, whereas, vasodilatory responsiveness to vasodilators (Ach, thrombin, adenosine, and SNP) showed no significant changes as compared with that in control rats. It has also been found that the endothelium has an inhibitory modulatory influence on the vasoconstrictor responsiveness to 5-HT in basilar arteries, and the hyperreactivity to 5-HT in basilar arteries from simulated-microgravity rats may also be due to an impairment in this endothelial modulatory function. The results further suggest that substances like endothelium-derived hyperpolarizing factors (EDHF) are responsible for this endothelium-dependent attenuating modulatory mechanism in contractile responsiveness of rat basilar arteries to 5-HT.2. Results from RT-PCR demonstrated that mRNAs of angiotensin II receptors, AT,a, AT,b and AT, were expressed in carotid arteries, abdominal aorta and femoral arteries, whereas only mRNAs of AT,a and AT,b were expressed in bailar arteries. There were no significant differences between the simulated-microgravtiy and control rats in the expression of mRNAs of ATU, ATlb and AT2 in these arteries. Angiotensin II can evoke only contractile rather than vasodalitory responsiveness in basilar arterial rings which are mediated by AT, receptors. There were no significant differences in contractileresponsiveness induced by Angiotensin II between the simulated-microgravtiy and control rats.3. Daily exposure with different durations to head-up tilt (4 or 2 h), standing (4, 2, or 1 h) or centrifugation (1.5 or 2.6 G for 1 h/d) showed a counteracting effect in preventing the enhancement of contractile responsiveness in basilar arterial rings from simulated-microgravity rats. It has also been demonstrated that the hypertrophy of vascular wall with smooth muscle cell hyperplasia in rat basilar arteries resulted from 3-wk simulated microgravity can be prevented by daily 4-h exposure to head-up tilt.These findings about the structural and functional changes in cerebral arteries from simulated-microgravity rats have provided a strong evidence for the "peripheral e...
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