Chow S Y, Woodbury D M, Yen-Chow Y C
Department of Physiology, University of Utah School of Medicine, Salt Lake City 84108.
J Endocrinol. 1990 Oct;127(1):85-101. doi: 10.1677/joe.0.1270085.
Mechanisms of pH recovery after alkalinization and acidification by exposing or prepulsing turtle thyroid slices with a Hanks' balanced salt solution (HBSS) containing NH4Cl or CO2 were studied by examining the effects of amiloride, 4-acetamido-4'-isocyanostilbene-2,2'-disulphonic acid (SITS), frusemide and acetazolamide, and of reducing the concentration of Na+ or Cl- in the incubation medium. When alkalinization was produced either during exposure to NH4Cl or after a CO2 pulse, the pH in thyroid slices rose rapidly and then recovered gradually. Addition of SITS (0.1 mmol/l) or reduction of the Cl- concentration markedly inhibited pH recovery. However, amiloride (0.1 mmol/l) and low Na+ in the medium had no significant effect on recovery from alkalinization induced by NH4Cl exposure or by a CO2 pulse. These data suggest that pH recovery from alkalinization in turtle thyroid gland is achieved by an exchange of internal HCO3- for external Cl-. When acidification was accomplished by either exposure to CO2 or removal of NH4Cl, the pH of thyroid slices fell rapidly and then recovered gradually. If amiloride was added or the Na+ concentration in the medium was reduced, the pH recovery was greatly attenuated. However, SITS and low Cl- in the medium did not affect the recovery from an acid load in turtle thyroid slices. These results suggest that pH recovery from acidification in turtle thyroid gland is achieved by an exchange of internal H+ for external Na+. Both frusemide and acetazolamide prevented the pH recovery in turtle thyroid slices during exposure to and withdrawal from NH4Cl. These results suggest that besides the Na(+)-H+ and Cl(-)-HCO3- exchange processes, other mechanisms may also be involved in pH regulation in turtle thyroid glands. Simultaneous uptakes into turtle thyroid slices of 125I- and 22Na+ and of 125I- and 36Cl- were studied during and following exposure to NH4Cl in the absence and presence of different transport inhibitors, such as frusemide, amiloride, SITS and acetazolamide. When the thyroid slices were exposed to HBSS containing 30 mmol/l NH4Cl (alkalinization phase), the tissue/medium (T/M) ratios of 125I- increased gradually, reached the highest point in 10 min, and were maintained at this level for the next 20 min. The T/M ratios of 22Na+ and 36Cl- of thyroid slices also slowly increased after exposure to NH4Cl.(ABSTRACT TRUNCATED AT 400 WORDS)
通过用含氯化铵(NH₄Cl)或二氧化碳(CO₂)的汉克斯平衡盐溶液(HBSS)处理或预脉冲龟甲状腺切片来碱化和酸化后,研究pH恢复机制。通过检测氨氯吡咪、4-乙酰氨基-4'-异氰基芪-2,2'-二磺酸(SITS)、呋塞米和乙酰唑胺的作用,以及降低孵育培养基中Na⁺或Cl⁻的浓度来进行研究。当在暴露于NH₄Cl期间或CO₂脉冲后产生碱化时,甲状腺切片中的pH迅速上升,然后逐渐恢复。添加SITS(0.1 mmol/L)或降低Cl⁻浓度显著抑制pH恢复。然而,氨氯吡咪(0.1 mmol/L)和培养基中低Na⁺对NH₄Cl暴露或CO₂脉冲诱导的碱化恢复没有显著影响。这些数据表明,龟甲状腺中碱化后的pH恢复是通过内部HCO₃⁻与外部Cl⁻交换实现的。当通过暴露于CO₂或去除NH₄Cl实现酸化时,甲状腺切片的pH迅速下降,然后逐渐恢复。如果添加氨氯吡咪或降低培养基中Na⁺浓度,pH恢复会大大减弱。然而,SITS和培养基中低Cl⁻并不影响龟甲状腺切片酸负荷后的恢复。这些结果表明,龟甲状腺中酸化后的pH恢复是通过内部H⁺与外部Na⁺交换实现的。呋塞米和乙酰唑胺在暴露于NH₄Cl期间和从NH₄Cl中撤出时均阻止了龟甲状腺切片的pH恢复。这些结果表明,除了Na⁺-H⁺和Cl⁻-HCO₃⁻交换过程外,其他机制可能也参与龟甲状腺的pH调节。在不存在和存在不同转运抑制剂(如呋塞米、氨氯吡咪、SITS和乙酰唑胺)的情况下,研究了在暴露于NH₄Cl期间及之后龟甲状腺切片对¹²⁵I⁻和²²Na⁺以及¹²⁵I⁻和³⁶Cl⁻ 的同时摄取。当甲状腺切片暴露于含30 mmol/L NH₄Cl的HBSS(碱化阶段)时,¹²⁵I⁻的组织/培养基(T/M)比值逐渐增加,在10分钟时达到最高点,并在接下来的20分钟内保持在该水平。甲状腺切片的²²Na⁺和³⁶Cl⁻的T/M比值在暴露于NH₄Cl后也缓慢增加。(摘要截短于400字)