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

我们研究了细胞Ca^<2+>运动及其在阻力血管平滑肌收缩舒张调控中的作用。主要帮助如下：1。跨膜钙<2+>内流与细胞内钙<2+>释放的关系。基于Ca^<2+>诱导经40mMK^+， Ca^<2+>无介质去极化的大鼠肠系膜阻力血管收缩对ryanodine的敏感性，表明Ca^<2+>通过Ca^<2+>通道内流触发Ca^<2+>从肌浆网释放。这种机制在生理学上可能是重要的，因为它将收缩的阈值水平放大到最大水平的一半。另一方面，在静息状态下，肌浆网起到缓冲胞质Ca^<2+>的汇作用。用赖诺定去除这一功能会引起张力的发展。2. 高血压血管静息状态下细胞质Ca^<2+>水平升高及Ca^<2+>依赖性K^+通道的激活。自发性高血压大鼠（SHR）对洗浴液中去除Ca^<2+>或Ca^<2+>通道阻滞剂的张力下降更大，对白蜡毒素和Ca^<2+>激活的K^+通道阻滞剂的收缩反应更大。用fura-2测定细胞质Ca^<2+>显示SHR血管中Ca^<2+>的静息水平较高。静息膜电位在高血压血管和正常血管之间没有差异。提示Ca^<2+>在静息状态下容易进入SHR血管细胞，从而产生主动张力，激活Ca^<2+>激活的K^+通道。肾上腺素能受体激活引起的强直性收缩的性质。我们对α 1受体激动剂苯肾上腺素引起的强直性收缩进行了分析，发现其收缩由两部分组成，一是与蛋白激酶C的活化有关，二是依赖于Ca^<2+>通道通过l型Ca^<2+>通道内流。前者可能导致收缩系统对Ca^<2+>的灵敏度增加。目前还在研究是否同样的机制是α - 1肾上腺素能受体介导的阻力血管收缩的基础。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