Zadunaisky J A
Department of Physiology and Neuroscience, New York University Medical Center, New York, USA.
Kidney Int. 1996 Jun;49(6):1563-7. doi: 10.1038/ki.1996.225.
The chloride cells of the gill secretory epithelium of fish that make the transition from fresh water to sea water adapt to the increased salinity by responding to a rapid signal that stimulates chloride secretion. In this paper, data are presented supporting the view that the transient increase in plasma osmolarity that can be measured during the transition is responsible for the stimulation of chloride secretion. A maximal increase of 65 mOsm in the plasma of Fundulus heteroclitus (the killifish) was found during acclimation to sea water. Similar or greater increases of osmolarity induced by mannitol on the basolateral side of isolated opercular epithelial membranes of the same species of fish containing great numbers of chloride cells produced stimulation of chloride secretion detected as the short circuit current. The shrinkage of the chloride cell activates the Na-K-2Cl cotransporter, and the Na/H exchanger and requires the integrity of apical chloride channels and normal levels of Ca. A Cl/HCO3 exchanger did not participate in this osmotic response to higher salinity. Chloride cell volume responses to osmolarity were studied with imagine and quantitative optics.
从淡水过渡到海水的鱼类鳃分泌上皮中的氯化物细胞，通过对刺激氯化物分泌的快速信号作出反应，来适应盐度的增加。本文提供的数据支持这样一种观点，即在过渡期间可测量到的血浆渗透压的短暂升高是刺激氯化物分泌的原因。在将底鳉（鳉鱼）适应海水的过程中，发现其血浆渗透压最大增加了65毫渗摩尔。用甘露醇在同一物种含有大量氯化物细胞的分离鳃盖上皮膜的基底外侧诱导的渗透压类似或更大的增加，会产生作为短路电流检测到的氯化物分泌刺激。氯化物细胞的收缩激活了钠 - 钾 - 2氯协同转运蛋白和钠/氢交换器，并且需要顶端氯化物通道的完整性和正常水平的钙。氯/碳酸氢根交换器不参与对更高盐度的这种渗透反应。用成像和定量光学方法研究了氯化物细胞体积对渗透压的反应。
