Sato K, Yamazaki J, Nagao T
Laboratory of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Japan.
Am J Physiol. 1998 Feb;274(2):H494-9. doi: 10.1152/ajpheart.1998.274.2.H494.
The vascular tension in the coronary artery is modulated by factors released by endothelial cells. We investigated the relationship between the Ca2+ level in endothelium and endothelium-mediated changes in smooth muscle tone in high K(+)-depolarized canine coronary arteries by measuring intracellular Ca2+ concentration fluorimetrically with the Ca2+ indicator fura 2. Addition of Ca2+ (1 mM) caused an increase in endothelial Ca2+ and relaxed the 30 mM K(+)-depolarized arteries following inhibition of Ca2+ influx in the smooth muscle with diltiazem. This relaxation was inhibited by NG-monomethyl-L-arginine. As extracellular K+ concentration was decreased, increases of endothelial Ca2+ were augmented, whereas the relaxation was decreased. Basal muscle tone was found to be decreased in low K+ by measuring relaxation by sodium nitroprusside. These results suggest the importance of Ca2+ level in the endothelium in playing a modulatory role in coronary tension through the production of nitric oxide. The correlation of extracellular K+ to Ca2+ level in the endothelium indicates a typical characteristic of the passive Ca2+ entry pathway in the endothelium, whereas the resultant relaxation appears to be restricted by the basal muscle tone.
冠状动脉中的血管张力受内皮细胞释放的因子调节。我们通过使用钙离子指示剂fura 2以荧光法测量细胞内钙离子浓度，研究了高钾（K⁺）去极化犬冠状动脉中内皮细胞内钙离子水平与内皮介导的平滑肌张力变化之间的关系。加入钙离子（1 mM）会导致内皮细胞内钙离子增加，并在使用地尔硫卓抑制平滑肌细胞内钙离子内流后，使30 mM钾（K⁺）去极化的动脉舒张。这种舒张作用被N⁺-单甲基-L-精氨酸抑制。随着细胞外钾（K⁺）浓度降低，内皮细胞内钙离子的增加增强，而舒张作用减弱。通过测量硝普钠引起的舒张作用，发现低钾时基础肌张力降低。这些结果表明，内皮细胞内钙离子水平通过产生一氧化氮在调节冠状动脉张力中起重要作用。细胞外钾（K⁺）与内皮细胞内钙离子水平的相关性表明了内皮细胞中钙离子被动内流途径的典型特征，而由此产生的舒张作用似乎受到基础肌张力的限制。
