Sutudy of vascular reactions in response to hemodynamic factors assessed by stretch activation

脑动脉和冠状动脉对血流动力学因素，即生物动力性刺激，包括血压和血流极为敏感。我从以下角度研究了心血管系统机械接收的ca^<2+>-信号机制，作为领导者推动了这一相对不发达的研究领域的进展。笔者认为血管对血管壁拉伸或腔内压力升高的肌源性收缩反应是一种细胞/细胞内和Ca^<2+>信号；3)收缩单元的跨桥性。我本可以展示如下有趣的结果，这将为未来的研究进展提供希望。我发现膜流动性强烈影响机械受体部位的敏感性，而一种阿米洛利敏感成分，一种可能的拉伸激活通道，可能在肌生成活动的发生中发挥作用。此外，生物力学刺激增强了磷脂酶C的活性、肌醇三磷酸的产生以及细胞质Ca^<2+>浓度的增加，这表明gtp结合蛋白与该酶偶联可能在机械刺激向细胞信号转化的过程中发挥作用。此外，在跨桥循环的性质中，发现肌生成活动介于佛波酯和高K^+去极化刺激产生的收缩之间。这些结果表明，血管对生物力学刺激的反应是通过一种新的细胞信号传导机制介导的。

Cerebral and coronary arteries are extremely sensitive to hemodynamic factors, i.e., biomichacal stimule, including blood pressure and blood flow. I have investigated the ca^<2+>-signaling mechanisms of mechanical reception in the cardiovascular system from the following point of view, and as a leader i have promoted the progress of this relatively underdeveloped research field. I have regarded the myogenic contractile reaction of blood vessels in response to stretch of vascular wall or an increase in intraluminal pressure as a kind of cellular/intracellular and Ca^<2+> signaling ; and 3) the cross-bridge property of contractile elements. I could have showed interesting results as follows which will promise the future progress in the research. I have found that membrane fluidity strongly affects the sensitivity of a mechano-receptor site, and an amiloride-sensitive component, a possible stretch-activated channel, may play a role in the genesis of myogenic activity. In addition, the biomechanical stimulus augmented the activity of phospholipase C, production of inositol trisphosphate, and increase in cytosolic Ca^<2+> concentration, which indicates a possible role of GTP-binging proteins coupled with this enxyme in the transformation of mechanical stimulus to cellular signalings. Moreover, myogenic activity is found to be in-between the contraction produced by phorbol esters and high K^+ depolarizing stimulus in the property of cross-bridge cycling. These results suggest that vascular reaction in response to biomechanical stimuli is mediated through a novel mechanisum of cellular signaling.