Suzuki Hikaru, Kito Yoshihiko, Fukuta Hiroyasu, Yamamoto Yoshimichi
Department of Physiology, Nagoya City University Medical School, Nagoya, Japan.
J Smooth Muscle Res. 2002 Apr;38(1-2):23-37. doi: 10.1540/jsmr.38.23.
The effects of cyclopiazonic acid (CPA), a known Ca2+-pump inhibitor at internal stores, were investigated on electrical responses of the membrane of smooth muscle cells in small segments (0.3-0.5 mm long) of circular smooth muscle isolated from the guinea-pig gastric antrum. In most preparations, the membrane was spontaneously active with the generation of unitary potentials and regenerative slow potentials. Low concentrations (< 1 microM) of CPA did not alter either the membrane potential or the amplitude and frequency of slow potentials. CPA at a concentration of 1 microM initially increased the frequency of slow potentials, but this was followed by a decrease in the frequency as a result of sustained exposure to CPA, with no alteration of either the membrane potential or the amplitude of slow potentials. Higher concentrations of CPA (2-5 microM) depolarized the membrane and decreased the amplitude and frequency of slow potentials. CPA at higher than 10 microM abolished slow potentials with depolarization of the membrane. Intracellular electrical responses recorded simultaneously from paired cells were synchronized, indicating electrical coupling of the cells. Depolarization of the membrane with current stimuli through one electrode evoked regenerative slow potentials superimposed on the electrotonic potentials. The evoked slow potential had a refractory period of about 7 s. CPA (up to 10 microM) did not prevent the synchronization of paired cells. The refractory period for slow potentials was reduced by low concentrations of CPA (< 1 microM) and increased by higher concentrations of CPA (2-10 microM). These results suggest that lower concentrations of CPA produce excitatory actions on gastric smooth muscles due to a secondary effect of increased intracellular [Ca2+], while higher concentrations of CPA produce inhibitory actions as a result of reduced release of Ca2+ from depleted internal stores.
研究了环匹阿尼酸(CPA)对从豚鼠胃窦分离的环形平滑肌小段(0.3 - 0.5毫米长)平滑肌细胞膜电反应的影响,CPA是一种已知的内质网Ca²⁺泵抑制剂。在大多数标本中,细胞膜自发活动,产生单位电位和再生性慢电位。低浓度(<1微摩尔)的CPA既不改变膜电位,也不改变慢电位的幅度和频率。1微摩尔浓度的CPA最初增加慢电位频率,但持续暴露于CPA后频率下降,而膜电位和慢电位幅度均无改变。较高浓度的CPA(2 - 5微摩尔)使膜去极化,并降低慢电位的幅度和频率。高于10微摩尔的CPA使膜去极化并消除慢电位。从配对细胞同时记录的细胞内电反应是同步的,表明细胞间存在电偶联。通过一个电极施加电流刺激使膜去极化,诱发的再生性慢电位叠加在电紧张电位上。诱发的慢电位有大约7秒的不应期。CPA(高达10微摩尔)并不阻止配对细胞的同步。低浓度(<1微摩尔)的CPA缩短慢电位的不应期,而较高浓度(2 - 10微摩尔)的CPA延长不应期。这些结果表明,较低浓度的CPA由于细胞内[Ca²⁺]增加的继发效应而对胃平滑肌产生兴奋作用,而较高浓度的CPA由于内质网Ca²⁺释放减少而产生抑制作用。