Hayashida N, Okui K, Fukuda Y
Jpn J Physiol. 1986;36(4):783-94. doi: 10.2170/jjphysiol.36.783.
The mechanism of spontaneous contraction of vascular smooth muscles in the elastic artery was studied in a ring-shaped preparation isolated from the rat aorta. The observation of small changes in vascular tension with a high gain AC amplification of tension signal provided a reliable detection of spontaneous contractions. The spontaneous rhythmic contraction (RC) occurred consistently in the preparation taken from the thoracic aorta without external stimuli. The RC (frequency, 5-20 cycle/min; amplitude, 10-100 mg) was accompanied with small oscillatory changes in the membrane potential (2-5 mV, peak to peak). A reduction in temperature (below 30 degrees C) or superfusing the preparation with Ca-free solution inhibited the generation of RC. Ca-entry blockers (verapamil and nifedipine) also inhibited the RC. The cessation of RC by these procedures reduced the vascular tension by about 40% of control baseline tension. The application of adrenergic blockers had little effect on the pattern of RC and on the vascular tension. The results suggest that the RC is generated by a synchronization of electrical and mechanical activities in relatively small groups of smooth muscle cells, which depends upon the temperature and requires the Ca-entry into the cells. The process of initiation of spontaneous RC in the rat aorta was discussed.
在从大鼠主动脉分离出的环形标本中研究了弹性动脉血管平滑肌的自发收缩机制。通过对张力信号进行高增益交流放大来观察血管张力的微小变化,从而可靠地检测出自发收缩。在没有外部刺激的情况下,取自胸主动脉的标本中持续出现自发节律性收缩(RC)。RC(频率为5 - 20次/分钟;幅度为10 - 100毫克)伴随着膜电位的小振荡变化(峰峰值为2 - 5毫伏)。温度降低(低于30摄氏度)或用无钙溶液灌流标本会抑制RC的产生。钙通道阻滞剂(维拉帕米和硝苯地平)也抑制RC。通过这些操作使RC停止会使血管张力降低至对照基线张力的约40%。应用肾上腺素能阻滞剂对RC模式和血管张力几乎没有影响。结果表明,RC是由相对小群的平滑肌细胞中电活动和机械活动的同步产生的,这取决于温度且需要钙离子进入细胞。讨论了大鼠主动脉中自发RC的起始过程。