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首页> 外文期刊>Japanese Journal of Pharmacology >Adrenergic Receptor-Mediated Cl- Transport in Rabbit Corneal Endothelial Cells
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Adrenergic Receptor-Mediated Cl- Transport in Rabbit Corneal Endothelial Cells

机译：肾上腺素受体介导的兔角膜内皮细胞Cl-转运

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References(20) Cited-By(2) Adrenoceptor-mediated Cl- transport in cultured rabbit corneal endothelium was examined using a Cl--sensitive fluorescent dye. The intracellular Cl- concentration ([Cl-]i) in the endothelial cells was estimated to be about 30 mM. Noradrenaline (0.001-0.1 mM) transiently decreased the [Cl-]i in a dose-dependent manner. Such a decrease in [Cl--]i was completely antagonized by pretreatment with the α-adrenoceptor antagonist phentolamine (0.1 mM). The selective α2-adrenoceptor agonist UK 14304-18 (5-bromo-6-[(4H, 5H-imidazol-2-yl)amino]quinoxaline, 0.1 mM) persistently decreased the [Cl-]i, but neither the α1-adrenoceptor agonist phenylephrine (0.1 mM) nor the β-adrenoceptor agonist isoproterenol (0.1 mM) had any effect. The α2-adrenoceptor agonist/antagonist yohimbine (0.1 mM) persistently and more strongly decreased the [Cl-]i than UK 14304-18 did. The yohimbine-induced decrease in the [Cl-]i was not further altered by UK 14304-18 or phenylephrine, but partly reversed by noradrenaline, isoproterenol and an adenylate cyclase activator, forskolin (0.1 mM). The yohimbine-induced decrease in [Cl-]i was inhibited by the carbonic anhydrase inhibitor acetazolamide (1 mM), and Cl--/HC03- exchange inhibitors, 4-acetamido-4'' -isothiocyanostilbene-2, 2'' disulfonic acid and 4, 4'' -diisothiocyanostilbene-2, 2''-disulfonic acid, but not by the H+-ATPase inhibitor N, N'' dicyclohexylcarbodiimide. The forskolin-induced recovery in [Cl-]i was inhibited by the Na+/K+/Cl- cotransport inhibitor bumetanide (0.1 mM), but not by the Cl-channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoic acid. These findings suggest that corneal endothelial cells extrude Cl- upon α2-adrenoceptor stimulation and accumulate Cl- upon β-adrenoceptor stimulation under low [Cl-]i conditions, probably via acceleration of Cl-/HC03- exchange and Na+/K+/ Cl- cotransport, respectively.
机译：参考文献（20）用Cl敏感的荧光染料检查了培养的兔角膜内皮中被Cy-By（2）介导的肾上腺素受体介导的Cl转运。内皮细胞中的细胞内Cl-浓度（[Cl-] i）估计为约30mM。去甲肾上腺素（0.001-0.1 mM）以剂量依赖性方式暂时降低[Cl-] i。通过用α-肾上腺素受体拮抗剂苯妥拉明（0.1 mM）进行预处理，可以完全拮抗[Cl-] i的这种下降。选择性α2-肾上腺素受体激动剂UK 14304-18（5-bromo-6-[（4H，5H-咪唑-2-基）氨基]喹喔啉，0.1 mM）持续降低[Cl-] i，但α1-均不降低肾上腺素受体激动剂去氧肾上腺素（0.1 mM）或β肾上腺素受体激动剂异丙肾上腺素（0.1 mM）都没有作用。 α2-肾上腺素受体激动剂/拮抗剂育亨宾（0.1 mM）比UK 14304-18持久且更强烈地降低[Cl-] i。育亨宾诱导的[Cl-] i的降低并未被UK 14304-18或去氧肾上腺素进一步改变，但被去甲肾上腺素，异丙肾上腺素和腺苷酸环化酶激活剂forskolin（0.1 mM）所部分逆转。育亨宾诱导的[Cl-] i的降低被碳酸酐酶抑制剂乙酰唑胺（1 mM）和Cl-/ HC03-交换抑制剂，4-乙酰氨基-4''-异硫氰基茂铁2，2''二磺酸抑制酸和4，4''-二异硫氰基苯乙烯-2，2''-二磺酸，但不是由H + -ATPase抑制剂N，N''二环己基碳二亚胺形成。 Na + / K + / Cl-共转运抑制剂布美他尼（0.1 mM）抑制了福司可林诱导的[Cl-] i的回收，但Cl通道阻滞剂5-硝基-2-（3-苯基丙基氨基）-苯甲酸却没有抑制酸。这些发现表明，在低[Cl-] i条件下，角膜内皮细胞在α2-肾上腺素受体刺激下挤出Cl-，在β-肾上腺素受体刺激下积累Cl-，可能是通过加速Cl- / HC03-交换和Na + / K + / Cl-共同运输。

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