IONIC BASIS OF PACEMAKER GENERATION IN DOG COLONIC SMOOTH-MUSCLE
IONIC BASIS OF PACEMAKER GENERATION IN DOG COLONIC SMOOTH-MUSCLE
复制标题
DOI：
10.1113/jphysiol.1989.sp017767
复制
发表时间：
1989-09-01
影响因子：
5.5
通讯作者：
HUIZINGA, JD
中科院分区：
文献类型：
--
作者：
BARAJASLOPEZ, C;DENHERTOG, A;HUIZINGA, JD
1.慢波的离子基础的狗结肠的环形肌肉，特别是在其启动的离子电导，进行了研究，通过测量细胞内的电活动在Abe-Tomita型室的电压控制。2.启动慢波活动的去极化可以由内向电流的增加和/或外向电流的阻断引起。根据以前的工作，内向电流可以由Na+，Cl-和Ca 2+离子携带; K+离子将携带外向电流。3. Na+通道阻断剂河豚毒素（5 × 1000 μ g/ml）在100 ℃下孵育。10-7 M）不影响慢波振幅及其上升速率。省略Na+后，用N-甲基-D-葡糖胺代替Na+，大的慢波继续发展，尽管慢波特征发生了一些变化。4.用羟乙基磺酸盐取代91%的Cl-可降低慢波频率，增加慢波振幅。而蔗糖替代NaCl则使慢波频率增加，振幅减小. 5. D 600（10-6 M）或CoCl 2（1-3 mM）阻断Ca 2+内流后，慢波活动继续发展。D_（600）和Co ~（2+）对膜电位无影响，但使慢波振幅降低，平台电位消失。忽略细胞外Ca ~（2+）（加1 mM-EGTA）后，慢波消失。这表明，Ca 2+内流可能是不必要的，但细胞外的Ca 2+离子的存在是必不可少的慢波产生。6.通过用Li+代替Na+，0 Na+、Li+ HEPES溶液加上D 600的组合使细胞去极化（高达约0.001）。-40 mV），并消除慢波活动。这种效应是电压依赖性的，因为复极化引起慢波返回。7.通过电流诱导的去极化至apprx也获得了慢波活动的消除。-40 mV。然而，在高K+诱导的去极化（至apprx. -40 mV）高振幅（16 mV）慢波仍然存在，表明慢波的电压依赖性正移。这种效应可能是由于细胞外K+对电压依赖性K+电导的修饰而发生的，这表明K+电导参与了慢波的产生。8.总之，慢波产生的周期性膜电导的变化，这是依赖于细胞外Ca 2+离子的存在和膜电位。我们的数据是一致的假设，慢波是由封锁的K+电导。
1. The ionic basis of the slow waves in the circular muscle of the dog colon, in particular the ionic conductances involved in their initiation, were investigated by measuring intracellular electrical activity in the Abe-Tomita-type chamber for voltage control. 2. The depolarization that initiates the slow wave activity could be evoked by an increase in inward current and/or by a block of outward current. According to previous work, inward current could be carried by Na+, Cl-, and Ca2+ ions; K+ ions would carry outward current. 3. The Na+ channel blocker tetrodotoxin (5 .times. 10-7 M) did not affect the slow wave amplitude nor its rate of rise. After omission of Na+, by replacing Na+ with N-methyl-D-glucamine, large slow waves continued to develop although some changes in slow wave characteristics occurred. 4. Replacement of 91% of the Cl- by isethionate decreased the slow wave frequency and increased the slow wave amplitude. However, NaCl substitution by sucrose increased the slow wave frequency and decreased the slow wave amplitude. 5. Slow wave activity continued to develop after blockade of Ca2+ influx by D600 (10-6 M) or CoCl2 (1-3 mM). D600 and Co2+ did not affect the membrane potential but reduced the slow wave amplitude and abolished the plateau potential. Slow waves were abolished after omission of extracellular Ca2+ (plus 1 mM-EGTA). This suggests that Ca2+ influx is probably not necessary but extracellular presence of Ca2+ ions is indispensible for the slow wave generation. 6. The combination of 0 Na+, Li+ HEPES solution, by replacing Na+ with Li+, plus D600 depolarized the cells (up to .apprx. -40 mV) and abolished slow wave activity. This effect was voltage dependent since repolarization caused slow waves to return. 7. Abolition of the slow wave activity was also obtained by current-induced depolarization to .apprx. -40 mV. However, during high-K+-induced depolarization (to .apprx. -40 mV) high amplitude (16 mV) slow waves were still present, showing that the voltage dependence of the slow waves was shifted positively. This effect probably occurs due to modification by extracellular K+ of a voltage-dependent K+ conductance, which would suggest that a K+ conductance is involved in slow wave generation. 8. In conclusion, slow waves are generated by cyclic membrane conductance changes, which are dependent on the presence of extracellular Ca2+ ions and on the membrane potential. Our data are consistent with the hypothesis that slow waves are initiated by the blockade of a K+ conductance.