2 STABLE LEVELS OF DIASTOLIC POTENTIAL AT PHYSIOLOGICAL K+ CONCENTRATIONS IN HUMAN VENTRICULAR MYOCARDIAL-CELLS
2 STABLE LEVELS OF DIASTOLIC POTENTIAL AT PHYSIOLOGICAL K+ CONCENTRATIONS IN HUMAN VENTRICULAR MYOCARDIAL-CELLS
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DOI：
10.1161/01.res.66.1.191
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发表时间：
1990-01-01
影响因子：
20.1
通讯作者：
SINGER, DH
中科院分区：
文献类型：
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作者：
MCCULLOUGH, JR;CHUA, WT;SINGER, DH
当体外暴露于4 mM K+时，人心室的许多样本中的细胞可以表现出两种稳定水平的舒张电位（DP）中的任一种（即，-78。+-。4 mV或-45.+-。5 mV，平均值±。SEM）。在本报告中，我们表明，当浴K+浓度（Kb+）从4到7 mM升高时，某些部分去极化的人心室肌细胞的DP产生了持续的25-35 mV超极化（n=28）。当Kb+返回到4 mM时，大多数（但不是全部）这些细胞的DP恢复到原来的去极化水平。在其他细胞中，两个水平的DP之间的过渡发生在可变的Kb+范围从1到20 mM。我们调查的离子机制（S）之间的位移电位的两个水平的基础上，通过研究的部分去极化细胞在22个标本的人心室DP的K+依赖性。DP超极化平均为25.6 mV（从-44.4 ±. 1.3至-70.0.+-。1.3 mV;当Kb+从4增加到7 mM时，n=25）。通过K+-选择性微电极测定的细胞内K+活性在其它哺乳动物物种的正常报道范围内（106.7 ± 0.01）。4.4 4 mM K+中的mM; n=22），并且不受增加Kb+至7 mM的影响（111.7 ± 0.001）。6.6 mM; n=6）。Ba 2+（0.05 mM），一种内向整流K+电流的阻断剂，可逆地阻止了超极化，而乙酰毒毛旋花子苷（9 μ M）不能抑制它。从DP的超极化水平的去极化的离子基础也进行了研究。降低浴Na+浓度和暴露于30 μ M河豚毒素不能阻止去极化。而2 mM Mn ~（2+）则可抑制去极化。这些结果表明，去极化可能是由于Mn 2+敏感的内向电流。
Cells in many specimens of human ventricle can exhibit either of two stable levels of diastolic potential (DP) when exposed to 4 mM K+ in vitro (i.e., -78.+-.4 mV or -45.+-.5 mV, mean.+-.SEM). In this report we show that the DP of some partially depolarized human ventricular cells developed a sustained 25-35 mV hyperpolarization (n=28) when bath K+ concentration (Kb+) was raised from 4 to 7 mM. On return of Kb+ to 4 mM, the DP of most, but not all, of these cells returned to the original depolarized levels. In other cells, the transition between the two levels of DP occurred at variable Kb+ ranging from 1 to 20 mM. We investigated the ionic mechanism(s) underlying the shifts between the two levels of potential by studying the K+ dependence of the DP in partially depolarized cells in 22 specimens of human ventricle. DP hyperpolarized an average of 25.6 mV (from -44.4.+-.1.3 to -70.0.+-.1.3 mV; n=25) when Kb+ was increased from 4 to 7 mM. Intracellular K+ activity, determined by K+-selective microelectrodes, was within the range of normal reported for other mammalian species (106.7.+-.4.4 mM in 4 mM K+; n=22) and was unaffected by increasing Kb+ to 7 mM (111.7.+-.6.6 mM; n=6). Ba2+ (0.05 mM), a blocker of the inward rectifying K+ current, reversibly prevented the hyperpolarization, whereas acetylstrophanthidin (9 .mu.M) failed to inhibit it. These results suggest that the hyperpolarization was due to a K+-dependent increase in K+ permeability and that electrogenic sodium pumping did not contribute significantly to the process. The ionic basis of the depolarization from a hyperpolarized level of DP also was investigated. Decreasing bath Na+ concentration and exposure to 30 .mu.M tetrodotoxin did not prevent the depolarization. However, the depolarization could be inhibited by 2 mM mn2+. These findings suggest that the depolarization may have been due to a Mn2+-sensitive inward current.