Zadunaisky J A, Cardona S, Au L, Roberts D M, Fisher E, Lowenstein B, Cragoe E J, Spring K R
Department of Physiology and Biophysics, New York University Medical Center, NY 10016, USA.
J Membr Biol. 1995 Feb;143(3):207-17. doi: 10.1007/BF00233449.
Transition from low salt water to sea water of the euryhaline fish, Fundulus heteroclitus, involves a rapid signal that induces salt secretion by the gill chloride cells. An increase of 65 mOsm in plasma osmolarity was found during the transition. The isolated, chloride-cell-rich opercular epithelium of sea-water-adapted Fundulus exposed to 50 mOsm mannitol on the basolateral side showed a 100% increase in chloride secretion, which was inhibited by bumetanide 10(-4) M and 10(-4) M DPC (N-Phenylanthranilic acid). No effect of these drugs was found on apical side exposure. A Na+/H+ exchanger, demonstrated by NH4Cl exposure, was inhibited by amiloride and its analogues and stimulated by IBMX, phorbol esters, and epithelial growth factor (EGF). Inhibition of the Na+/H+ exchanger blocks the chloride secretion increase due to basolateral hypertonicity. A Cl-/HCO3- exchanger was also found in the chloride cells, inhibited by 10(-4) M DIDS but not involved in the hyperosmotic response. Ca2+ concentration in the medium was critical for the stimulation of Cl- secretion to occur. Chloride cell volume shrinks in response to hypertonicity of the basolateral side in sea-water-adapted operculi; no effect was found on the apical side. Fresh-water-adapted fish chloride cells show increased water permeability of the apical side. It is concluded that the rapid signal for adaptation to higher salinities is an increased tonicity of the plasma that induces chloride cell shrinkage, increased chloride secretion with activation of the Na+K+2Cl- cotransporter, the Na+/H+ exchanger and opening of Cl- channels.
广盐性鱼类异齿底鳉从低盐度水过渡到海水，涉及一个快速信号，该信号可诱导鳃氯细胞分泌盐分。在过渡过程中，血浆渗透压增加了65毫渗摩尔。将适应海水的异齿底鳉分离出的富含氯细胞的鳃盖上皮细胞，在基底外侧暴露于50毫渗摩尔甘露醇时，氯分泌增加了100%，这被10⁻⁴ M布美他尼和10⁻⁴ M DPC（N-苯基邻氨基苯甲酸）抑制。在顶端暴露时未发现这些药物有任何作用。通过氯化铵暴露证明的Na⁺/H⁺交换体，被阿米洛利及其类似物抑制，并被异丁基甲基黄嘌呤、佛波酯和表皮生长因子（EGF）刺激。抑制Na⁺/H⁺交换体可阻断由于基底外侧高渗引起的氯分泌增加。在氯细胞中还发现了一种Cl⁻/HCO₃⁻交换体，被10⁻⁴ M DIDS抑制，但不参与高渗反应。培养基中的Ca²⁺浓度对于刺激Cl⁻分泌的发生至关重要。在适应海水的鳃盖中氯细胞体积会因基底外侧的高渗而缩小；在顶端未发现影响。适应淡水的鱼类氯细胞顶端的水通透性增加。结论是，适应更高盐度的快速信号是血浆张力增加，这会诱导氯细胞收缩，通过激活Na⁺K⁺2Cl⁻共转运体、Na⁺/H⁺交换体和打开Cl⁻通道来增加氯分泌。
