Altered Ca fluxes and contractile state during pH changes in cultured heart cells.
Altered Ca fluxes and contractile state during pH changes in cultured heart cells.
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培养心脏细胞 pH 值变化期间钙通量和收缩状态发生改变。
DOI：
10.1152/ajpcell.1987.253.1.c137
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
T. Smith
中科院分区：
文献类型：
--
作者：
D. Kim;T. Smith
我们利用培养的鸡胚心室细胞研究了细胞内（pHi）或细胞外（pHo）pH变化引起心肌收缩状态改变的机制。在HEPES缓冲液中，pHo从7.4变为6.0或8.8时，细胞运动幅度分别改变了 -85%或 +60%，10秒时的⁴⁵Ca摄取分别改变了 -29%或 +22%。pHo诱导的Ca摄取变化对硝苯地平（10 μM）不敏感，但依赖于Na⁺梯度。由NH₄Cl引起的pHi变化或在pH值为6.0 - 8.8的培养基中预孵育，未能显著改变⁴⁵Ca摄取或外流。然而，pHi的较大变化与Ca摄取改变有关。pHo从7.4变为6.0或8.8时，分别与⁴⁵Ca外流的初始变化 +17%或 -18%相关，且这些效应不依赖于Na⁺。细胞暴露于20 mM NH₄Cl会导致细胞内碱化和正性肌力作用，而随后去除NH₄Cl会引起细胞内酸化和负性肌力作用。然而，pHi和收缩状态之间缺乏紧密的时间关系。这些结果表明，在培养的心肌细胞中，pHo诱导的收缩状态变化与跨肌膜Ca²⁺运动的改变密切相关，并且可能（至少部分）是由于这些Ca²⁺通量变化所致。相比之下，pHi诱导的收缩状态变化似乎主要涉及细胞内Ca²⁺处理的改变和/或肌原纤维Ca²⁺敏感性的改变。
We studied mechanisms underlying changes in myocardial contractile state produced by intracellular (pHi) or extracellular (pHo) changes in pH using cultured chick embryo ventricular cells. A change in pHo of HEPES-buffered medium from 7.4 to 6.0 or to 8.8 changed the amplitude of cell motion by -85 or +60%, and 45Ca uptake at 10 s by -29 or +22%, respectively. The pHo-induced change in Ca uptake was not sensitive to nifedipine (10 microM), but was Na gradient dependent. Changes in pHi produced by NH4Cl or preincubation in media at pH values ranging from 6.0 to 8.8 failed to alter significantly 45Ca uptake or efflux. However, larger changes in pHi were associated with altered Ca uptake. Changes in pHo from 7.4 to 6.0 or to 8.8 were associated with initial changes in 45Ca efflux by +17 or -18%, respectively, and these effects were not Na dependent. Exposure of cells to 20 mM NH4Cl produced intracellular alkalinization and a positive inotropic effect, whereas subsequent removal of NH4Cl caused intracellular acidification and a negative inotropic effect. There was, however, a lack of close temporal relationship between pHi and contractile state. These results indicate that pHo-induced changes in contractile state in cultured heart cells are closely correlated with altered transsarcolemmal Ca movements and presumably are due (at least in part) to these Ca flux changes. In contrast, pHi-induced changes in contractile state appear principally to involve altered Ca handling within the cell and/or altered Ca sensitivity of myofibrils.