Sanders K M
Am J Physiol. 1983 May;244(5):C356-61. doi: 10.1152/ajpcell.1983.244.5.C356.
Sensitive mechanical and intracellular electrical recordings showed that phasic contractions occurred in response to electrical slow waves in the absence of Ca2+ action potentials. Drugs that either enhanced or depressed slow waves were used to study the relationship between slow-wave amplitude and the amplitude of the phasic contractions. Acetylcholine (Ach) (10(-8) to 3 X 10(-7) M) increased slow waves and contractions without causing action potentials. When ACh was raised to 10(-6) M, action potentials were elicited and accompanying contractions increased in amplitude by at least a factor of five. The Ca2+ channel blocker, Mn2+ (0.5 mM), decreased slow-wave amplitude and the associated phasic contractions. These data agree with a previous study (12), suggesting that an oscillation in intracellular Ca2+ occurs during each slow-wave cycle. The present study suggests that the increase in intracellular Ca2+ during the slow wave is sufficient to activate the contractile apparatus.
灵敏的机械和细胞内电记录显示,在没有Ca2+动作电位的情况下,相位性收缩是对电慢波的反应。使用增强或抑制慢波的药物来研究慢波振幅与相位性收缩振幅之间的关系。乙酰胆碱(Ach)(10^(-8)至3×10^(-7) M)增加慢波和收缩,而不引起动作电位。当Ach浓度提高到10^(-6) M时,引发动作电位,伴随的收缩振幅至少增加五倍。Ca2+通道阻滞剂Mn2+(0.5 mM)降低慢波振幅和相关的相位性收缩。这些数据与先前的一项研究(12)一致,表明在每个慢波周期内细胞内Ca2+发生振荡。本研究表明,慢波期间细胞内Ca2+的增加足以激活收缩装置。