The role of plasmalemmal Ca^<2+> channels and intracellular Ca^<2+> stores in vascular smooth muscles during the development of vascular resistance

本研究探讨了质膜Ca^2通道和肌浆网(SR)、细胞内Ca^2储存在血管平滑肌特别是阻力血管张力发展中的作用。主要研究结果如下：1)Ca^2通道和SR对细胞质Ca^2>([Ca^2>]i)的调节。我分析了SR功能调节剂兰尼碱和环吡阿尼酸对[Ca^2]i(用fura-2测量)和大鼠肠系膜阻力动脉张力的影响。结果表明，SR 在静息状态下充当减少 [Ca^<2>]i 的缓冲器，而当跨膜 Ca^<2> 流入增加时，它通过释放 Ca^<2> 来放大收缩。2) α1-肾上腺素受体激活后的 Ca^<2> 进入途径。当低浓度激动剂激活阻力血管的α1-肾上腺素受体时，通过电压依赖性Ca^2通道(VDC)的Ca^2流入增强，而没有任何去极化。这种流入触发了Ca^<2>从SR中释放。高浓度的激动剂引起去极化，这反过来又增强了Ca^<2>通过VDC的流入。除此之外，还发生了Ca^<2>通过VDC以外的途径进入。该条目对K 2 通道阻断剂敏感，但对二氢吡啶Ca 2 通道阻断剂不敏感。3)高血压血管中离子通道的功能。在自发性高血压的血管平滑肌中，电压依赖性Ca^2通道在静息状态下是活跃的，这产生主动张力并激活Ca^2激活的K^通道。增加的Ca ^ 2 流入向SR提供更多的Ca ^ 2 ，然后增加从SR释放的Ca ^ 2 。

In this study, the roles of plasmalemmal Ca^<2+> channels and sarcoplasmic reticulum (SR), intracellular Ca^<2+> stores, in the development of tension in vascular smooth muscle, especially in resistance vessels, were investigated. The major findings are as follws.1) Regulation of cytoplasmic Ca^<2+> ([Ca^<2+>]i) by Ca^<2+> channel and SR.I analyzed the effects of ryanodine and cyclopiazonic acid, modifiers of SR functions, on [Ca^<2+>]i, mesured with fura-2, and the tension of rat mesenteric resistance arteries. The results suggest that SR plays as a buffer to decrease [Ca^<2+>]i at a resting state, while it amplifies a contraction by releasing Ca^<2+> when transmembrane Ca^<2+> influx increased.2) Ca^<2+> entry pathways following activation of alpha1-adrenoceptor. When alpha1-adrenoceptors of resistance vassels was activated by low concentration of agonist, Ca^<2+> influx through voltage-dependent Ca^<2+> channel (VDC) was enhanced without any depolarization. This influx triggered Ca^<2+> release from SR.A high concentration of agonist caused depolarization, which in turn enhanced the Ca^<2+> influx through VDC.Besides this, Ca^<2+> entry through a pathway other than VDC also occurred. This entry was sensitive to K^+ channel blockers but not to dihydropyridine Ca^<2+> channel blockers.3) Functions of ion channels in the hypertensive vessels. In vascular smooth muscles from spontaneously hypertensive rate voltage-dependent Ca^<2+> channels were active at the resting state, which produced an active tension and activated Ca^<2+>-activated K^+ channels. Increased Ca^<2+> influx provided more Ca^<2+> to SR, then increased Ca^<2+> release from SR.