Cellular calcium movements and the role in regulating contraction and relaxation of vascular smooth muscles of resistance vessels

我们研究了阻力血管的血管平滑肌细胞内钙运动及其在收缩和松弛中的作用。主要的帮助如下：1.跨膜钙离子内流与细胞内钙离子释放的关系根据大鼠肠系膜阻力血管经40mMK~(2+)、Ca~(2+)去极化后对兰尼定的敏感性，结果表明，Ca~(2+)通过Ca~(2+)通道内流，触发肌浆网钙释放。这一机制可能在生理上很重要，因为它将收缩的阈值放大到一半最大。另一方面，在静息状态下，肌浆网起到了缓冲细胞质Ca~(2+)和Gt~(2+)的作用。Ryanodine去除这一功能导致了紧张的发展。2.高血压血管静息状态下胞浆Ca~(2+)和Gt~(2+)水平升高，激活Ca~(2+)依赖的K~(++)通道。股骨…与正常血压大鼠相比，自发性高血压大鼠(SHR)的More和颈动脉S对从浴液中去掉Ca~(2+)或Ca~(2+)通道阻滞剂的反应有更大的降压作用，而对河豚毒素和TEA、Ca~(2+)激活的K~(++)通道阻滞剂的收缩反应更强。Fura-2测定SHR血管胞浆Ca~(2+)和Gt~(2+)的静息水平显示SHR血管胞浆Ca~(2+)和Gt~(2+)的静息水平较高。静息膜电位在高血压血管和正常血压血管之间没有差别。提示静息状态下，钙离子容易进入自发性高血压大鼠血管内皮细胞，产生主动张力，激活钙离子激活的钾离子通道。由α-肾上腺素受体激活引起的紧张性收缩的本质。我们分析了α1受体激动剂苯肾上腺素引起的紧张性收缩，发现这种收缩由两种成分组成，一种与蛋白激酶C的激活有关，另一种依赖于通过L型钙通道的钙内流。前者可能导致收缩系统对Ca~(2+)的敏感性增加。目前正在研究是否有同样的机制存在于α1-肾上腺素受体介导的阻力血管收缩中。较少

We investigated the cellular Ca^<2+> Movement and its role in regulation of contractions and relaxations in vascular smooth muscles of resistance vessels. Major aidings are as follows.1. Relation of transmembrane Ca^<2+> influx to intracellular Ca^<2+> release. Based on the sensitivity to ryanodine of Ca^<2+>-induced contraction of rat mesenteric resistance vessels which had been depolarized by 40mMK^+, Ca^<2+>-free medium, it has been shown that Ca^<2+> influx through Ca^<2+> Channels triggers that Ca^<2+> release from sarcoplasmic reticulum. This mechanism may be physiologically important since it amplifies the threshold level of contraction to half maximal one. On the other hand, in resting state, the sarcoplasmic reticulum plays a role as a sink to buffer cytoplasmic Ca^<2+>. Removal of this function by ryanodine induced a tension development. 2. Increased level of cytoplasmic Ca^<2+> at resting state in hypertensive vessels and activation of Ca^<2+>-dependent K^+ channel. Femoral … More and carotid arterie s from spontaneously hypertensive rats(SHR)showed a greater decrease in tension in response to Ca^<2+>-removal from bathing solution or Ca^<2+> channel blockers and greater contractile responses to charybdotoxin and TEA, Ca^<2+>-activated K^+ channel blockers, than those from normotensive rats. Measurement of cytoplasmic Ca^<2+> with fura-2 revealed that the resting level of cytoplasmic Ca^<2+> was higher in SHR vessels. Resting membrane potential did not differ between hypertensive and normotensive vessels. It is suggested that Ca^<2+> easily enters cells in SHR vessels at resting state, thereby produces the active tension and activates Ca^<2+>-activated K^+ channels.3. The nature of tonic contraction induced by alpha-adrenoceptor activation. We analyzed the tonic contraction induced by phenylephrine, alpha1 receptor agonist, and found that the contraction was composed of two components, one is related to activation of protein kinase C and the other depends on Ca^<2+> influx through L-type Ca^<2+> channels. The former may cause an increase in the sensitivity to Ca^<2+> of contractile systems. It is under investigation whether the same mechanism underlies the alpha1-adrenoceptor mediated contraction of resistance vessels. Less