Behavior of junction channels between rat glomus cells during normoxia and hypoxia
Behavior of junction channels between rat glomus cells during normoxia and hypoxia
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DOI：
10.1152/jn.2002.88.2.639
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发表时间：
2002-08-01
影响因子：
2.5
通讯作者：
Eyzaguirre, C
中科院分区：
文献类型：
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作者：
Abudara, V;Jiang, RG;Eyzaguirre, C
采用双电压钳制法研究了大鼠颈动脉体血管球细胞在常氧（PO 2 300 Torr）和连二亚硫酸钠（Na 2S 2 O 4）或100%N-2诱导的缺氧条件下缝隙连接通道的活性。Na 2S 2 O 4将盐水PO 2减少到接近10 Torr，而100%N-2将环境O-2减少到接近60 Torr。提出了以下意见。1)在常氧条件下，细胞间宏电导（G（j）= 3.0+/-1.01 ns，平均值+/-SE）在缺氧条件下由任一试剂不均匀地改变（增加和减少），尽管N-2产生最大的变化。2)通道的细胞间微电导（g（j）= 104.44+/-10.16 pS在常氧条件下）在100%N-2中显著降低，但在Na 2S 2 O 4中显示出抑制和增强。3)单结通道（SCh）的电导，计算为g（j）方差/平均值g（j），得出的平均值为17.6 pS。手动测量数据获得的值更大（类似于34 pS）。当从数字化记录或手动测量计算时，缺氧性缺氧（由100%N-2诱导）显著抑制SCh的电导。Na_2S_2O_4引起的缺氧不显著改变连接电导。4)细胞间通道的数量以g（j）/SCh g（j）计算，平均值为452（范围1 ~ 2471）。在N-2诱导的缺氧过程中，这个数字显着下降到接近84，但在Na 2S 2 O 4缺氧过程中保持不变。5)在不同的实验中，连接通道的平均开放时间从4到30 ms不等，总体平均值为mu=11.33+/-0.33 ms。该值被100%N-2显著降低，但不被Na 2S 2 O 4改变。6)细胞内钙（[Ca 2 +]（i））在常氧下为46.2+/-4.84 nM，在Na 2S 2 O 4下显著增加至77.32+/-11.27 nM，在100%N-2下显著增加至66.39+/-11.64 nM。可以得出结论，100%N-2解偶联血管球细胞显着降低细胞间的宏观和微观电导。Na_2S_2O_4引起的缺氧有不同的影响。缺氧的偶联效应可能取决于[Ca 2 +]（i）的增加和/或细胞内pH值的变化，或受其辅助。然而，分泌的递质和ATP加上缺氧对第二信使和其他细胞质成分的影响也可能在这一现象中发挥重要作用。
The activity of gap junction channels between cultured and clustered carotid body glomus cells of the rat was studied with dual voltage clamping during normoxia (PO2 300 Torr) and hypoxia induced by sodium dithionite (Na2S2O4) or 100% N-2. Na2S2O4 reduced the saline PO2 to similar to10 Torr, whereas 100% N-2 reduced ambient O-2 to similar to60 Torr. The following observations were made. 1) In normoxia, the intercellular macroconductance (G(j) = 3.0+/-1.01 ns, mean+/-SE) was changed unevenly (increased and decreased) under hypoxic conditions by either agent, although N-2 produced the largest changes. 2) The intercellular microconductances of the channels (g(j) = 104.44+/-10.16 pS under normoxic conditions) significantly decreased in 100% N-2 but showed depressions and enhancements in Na2S2O4. 3) The conductance of single-junction channels (SChs), calculated as g(j) variance/mean g(j), yielded a mean of similar to17.6 pS. Larger values were obtained with manual measurements of the data (similar to34 pS). Hypoxic hypoxia (induced by 100% N-2) significantly depressed the conductance of SChs when calculated from digitized records or from manual measurements. Hypoxia induced by Na2S2O4 did not significantly change junctional conductance. 4) The number of intercellular channels, calculated as g(j)/SCh g(j), had a mean of similar to452 (range 1 to 2,471). During N-2-induced hypoxia, this number significantly decreased to similar to84 but remained unchanged during Na2S2O4 hypoxia. 5) The mean open time of junction channels varied from 4 to 30 ms in different experiments, having an overall mean of mu=11.33+/-0.33 ms. This value was significantly reduced by 100% N-2 but was not changed by Na2S2O4. 6) Intracellular calcium ([Ca2+](i)), 46.2+/-4.84 nM under normoxia, significantly increased to 77.32+/-11.27 nM with Na2S2O4 and to 66.39+/-11.64 nM with 100% N-2. It is concluded that 100% N-2 uncouples glomus cells by significantly reducing intercellular macro- and microconductances. Hypoxia induced by Na2S2O4 had variable effects. The coupling effects of hypoxia may depend on, or be aided by, increases in [Ca2+](i) and/or intracellular pH changes. However, secreted transmitters and ATP plus the effects of hypoxia on second messengers and other cytoplasmic components may also play an important role in this phenomenon.