Adrenergic receptor-mediated Cl- transport in rabbit corneal endothelial cells
| Autor: | Toshiko Mikami, Yoshito Mikami, Kyoko Omori, Xun-Ting Zeng, Masafumi Inoue, Mitsuyoshi Hara, Takao Irie, Chiyoko Inagaki, Masanobu Uyama, Akio Minato, Tohru Yasukura |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Agonist
medicine.medical_specialty Adrenergic Antagonists 4-Acetamido-4'-isothiocyanatostilbene-2 2'-disulfonic Acid medicine.drug_class 4 4'-Diisothiocyanostilbene-2 2'-Disulfonic Acid Acetates Photometry chemistry.chemical_compound Norepinephrine Phenylephrine Chlorides Internal medicine Quinoxalines medicine Na-K-Cl cotransporter Animals Channel blocker Phentolamine Ion transporter Cells Cultured Fluorescent Dyes Pharmacology Forskolin Ion Transport biology Dose-Response Relationship Drug Chemistry Colforsin Endothelium Corneal Isoproterenol Yohimbine Affinity Labels Adrenergic Agonists Receptors Adrenergic Acetazolamide Endocrinology Microscopy Fluorescence Brimonidine Tartrate biology.protein Quinolines Rabbits Cotransporter Bumetanide medicine.drug |
| Zdroj: | Japanese journal of pharmacology. 67(4) |
| ISSN: | 0021-5198 |
| Popis: | 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 α-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 α 1 -adrenoceptor agonist phenylephrine (0.1 mM) nor the β-adrenoceptor agonist isoproterenol (0.1 mM) had any effect. The α 2 -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 - /HCO 3 - 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 α 2 -adrenoceptor stimulation and accumulate Cl - upon β-adrenoceptor stimulation under low [Cl - ] i conditions, probably via acceleration of Cl - /HCO 3 - exchange and Na + /K + /Cl - cotransport, respectively |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|