Simchowitz L, Roos A
J Gen Physiol. 1985 Mar;85(3):443-70. doi: 10.1085/jgp.85.3.443.
The intracellular pH (pHi) of isolated human peripheral blood neutrophils was measured from the fluorescence of 6-carboxyfluorescein (6-CF) and from the equilibrium distribution of [14C]5,5-dimethyloxazolidine -2,4-dione (DMO). At an extracellular pH (pHo) of 7.40 in nominally CO2-free medium, the steady state pHi using either indicator was approximately 7.25. When pHo was suddenly raised from 7.40 to 8.40 in the nominal absence of CO2, pHi slowly rose by approximately 0.35 during the subsequent hour. A change of similar magnitude in the opposite direction occurred when pHo was reduced to 6.40. Both changes were reversible. Intrinsic intracellular buffering power, determined by using graded pulses of CO2 or NH4Cl, was approximately 50 mM/pH over the pHi range of 6.8-7.9. The course of pHi obtained from the distribution of DMO was followed during and after imposition of intracellular acid and alkaline loads. Intracellular acidification was brought about either by exposing cells to 18% CO2 or by prepulsing with 30 mM NH4Cl, while pHo was maintained at 7.40. In both instances, pHi (6.80 and 6.45, respectively) recovered toward the control value at rates of 0.029 and 0.134 pH/min. These rates were reduced by approximately 90% either by 1 mM amiloride or by replacement of extracellular Na with N-methyl-D-glucamine. Recovery was not affected by 1 mM SITS or by 40 mM alpha-cyano-4-hydroxycinnamate (CHC), which inhibits anion exchange in neutrophils. Therefore, recovery from acid loading is probably due to an exchange of internal H for external Na. Intracellular alkalinization was achieved by exposing the cells to 30 mM NH4Cl or by prepulsing with 18% CO2, both at a constant pHo 7.40. In both instances, pHi, which was 7.65 and 7.76, respectively, recovered to the control value. The recovery rates (0.033 and 0.077 pH/min, respectively) were reduced by 80-90% either by 40 mM CHC or by replacement of extracellular Cl with p-aminohippurate (PAH). SITS, amiloride, and ouabain (0.1 mM) were ineffective.(ABSTRACT TRUNCATED AT 400 WORDS)
通过6-羧基荧光素(6-CF)的荧光以及[14C]5,5-二甲基恶唑烷-2,4-二酮(DMO)的平衡分布来测量分离的人外周血中性粒细胞的细胞内pH值(pHi)。在名义上无二氧化碳的培养基中,细胞外pH值(pHo)为7.40时,使用任何一种指示剂测得的稳态pHi约为7.25。当在名义上无二氧化碳的情况下将pHo突然从7.40提高到8.40时,在随后的一小时内pHi缓慢上升约0.35。当pHo降至6.40时,会发生相反方向的类似幅度变化。两种变化都是可逆的。通过使用分级的二氧化碳或氯化铵脉冲测定,在6.8 - 7.9的pHi范围内,内在细胞内缓冲能力约为50 mM/pH。在施加细胞内酸和碱负荷期间及之后,跟踪由DMO分布获得的pHi变化过程。通过将细胞暴露于18%二氧化碳或用30 mM氯化铵预脉冲来实现细胞内酸化,同时将pHo维持在7.40。在这两种情况下,pHi(分别为6.80和6.45)以0.029和0.134 pH/分钟的速率恢复到对照值。1 mM氨氯吡咪或用N-甲基-D-葡糖胺替代细胞外钠可使这些速率降低约90%。1 mM SITS或40 mM α-氰基-4-羟基肉桂酸(CHC,抑制中性粒细胞中的阴离子交换)对恢复没有影响。因此,酸负荷后的恢复可能是由于细胞内的H与细胞外的Na进行交换。通过将细胞暴露于30 mM氯化铵或用18%二氧化碳预脉冲来实现细胞内碱化,两者均在恒定的pHo 7.40下进行。在这两种情况下,分别为7.65和7.76的pHi恢复到对照值。40 mM CHC或用对氨基马尿酸(PAH)替代细胞外氯可使恢复速率(分别为0.033和0.077 pH/分钟)降低80 - 90%。SITS、氨氯吡咪和哇巴因(0.1 mM)无效。(摘要截断于400字)