ADRENERGIC CONTROL OF RED CELL PH IN SALMONID FISH : ROLES OF THE SODIUM/PROTON EXCHANGE, JACOBS-STEWART CYCLE AND MEMBRANE POTENTIAL
ADRENERGIC CONTROL OF RED CELL PH IN SALMONID FISH : ROLES OF THE SODIUM/PROTON EXCHANGE, JACOBS-STEWART CYCLE AND MEMBRANE POTENTIAL
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鲑鱼红细胞 PH 的肾上腺素控制：钠/质子交换、雅各布斯-斯图尔特循环和膜电位的作用
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发表时间：
1990
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通讯作者：
Marita Paajaste
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作者：
M. Nikinmaa;K. Tiihonen;Marita Paajaste
我们研究了肾上腺素能激活钠/质子交换降低虹鳟红细胞膜pH梯度的机制。在未处理的细胞中，肾上腺素能刺激引起红细胞膜上质子分布比（[H+]e/[H+]i）显著增加。质子载体2，4-二硝基苯酚（2，4-DNP）可抑制肾上腺素能刺激引起的质子分配比增加。因此，钠/质子交换从电化学平衡中置换质子。通过钠/质子交换主动调节细胞内pH是可能的，因为碳酸到二氧化碳的细胞外脱水是未催化的。肾上腺素能刺激引起的质子分配比的增加在红细胞悬液中被抑制，其中细胞外碳酸酐酶在刺激前已被添加。与此相反，细胞内碳酸酐酶的抑制显着增加肾上腺素能刺激诱导的pH值的变化，这表明细胞内水合/脱水反应的净方向可能会显着影响细胞内的pH值的变化。膜电位变化不是肾上腺素能反应的必要组成部分。红细胞体积和钠和氯离子浓度的增加引起的肾上腺素能刺激不受细胞的电压钳位缬氨霉素。
We investigated the mechanisms by which adrenergic activation of sodium/proton exchange reduces the pH gradient across the membrane of rainbow trout red cells. In untreated cells, adrenergic stimulation caused a significant increase in the proton distribution ratio ([H+]e/[H+]i) across the red cell membrane. The increase in the proton distribution ratio caused by adrenergic stimulation was inhibited by the protonophore 2,4-dinitrophenol (2,4-DNP). Thus, sodium/proton exchange displaces protons from electrochemical equilibrium. Active regulation of intracellular pH by sodium/proton exchange is possible, because the extracellular dehydration of carbonic acid to carbon dioxide is uncatalyzed. The increase in proton distribution ratio caused by adrenergic stimulation was inhibited in red cell suspensions to which extracellular carbonic anhydrase had been added before stimulation. In contrast, inhibition of intracellular carbonic anhydrase markedly increased the pH changes induced by adrenergic stimulation, suggesting that the net direction of the intracellular hydration/dehydration reaction may markedly affect the intracellular pH changes. Membrane potential changes are not a necessary component of the adrenergic response. The increases in red cell volume and sodium and chloride concentrations induced by adrenergic stimulation were unaffected in cells ‘voltage-clamped’ by valinomycin.