Adrenergic receptor-mediated Cl- transport in rabbit corneal endothelial cells.
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 alpha-adrenoceptor antagonist phentolamine (0.1 mM). The selective alpha 2-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 alpha 1-adrenoceptor agonist phenylephrine (0.1 mM) nor the beta-adrenoceptor agonist isoproterenol (0.1 mM) had any effect. The alpha 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-/HCO3- 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'-dicylohexylcarbodiimide. 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.(ABSTRACT TRUNCATED AT 250 WORDS)
Yasukura
T
T
Department of Pharmacology, Kansai Medical University, Osaka, Japan.
Inoue
M
M
Irie
T
T
Hara
M
M
Mikami
Y
Y
Zeng
X T
XT
Mikami
T
T
Omori
K
K
Minato
A
A
Uyama
M
M
D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000494:pharmacology; D000085:Acetates / Q000378:metabolism; D000086:Acetazolamide / Q000494:pharmacology; D000322:Adrenergic Agonists / Q000494:pharmacology*; D018674:Adrenergic Antagonists / Q000494:pharmacology*; D000345:Affinity Labels / Q000494:pharmacology; D000818:Animals; D000068438:Brimonidine Tartrate; D002478:Cells, Cultured; D002712:Chlorides / Q000378:metabolism*; D005576:Colforsin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004728:Endothelium, Corneal / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D005456:Fluorescent Dyes / Q000737:chemistry; D017136:Ion Transport / Q000187:drug effects; D007545:Isoproterenol / Q000494:pharmacology; D008856:Microscopy, Fluorescence; D009638:Norepinephrine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D010783:Photometry; D011804:Quinolines / Q000737:chemistry; D011810:Quinoxalines / Q000494:pharmacology; D011817:Rabbits; D011941:Receptors, Adrenergic / Q000502:physiology*; D015016:Yohimbine / Q000494:pharmacology
D000085:Acetates; D000322:Adrenergic Agonists; D018674:Adrenergic Antagonists; D000345:Affinity Labels; D002712:Chlorides; D005456:Fluorescent Dyes; D011804:Quinolines; D011810:Quinoxalines; D011941:Receptors, Adrenergic; C078229:N-(6-methoxyquinolyl)acetoethyl ester; D005576:Colforsin; D010656:Phenylephrine; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D015016:Yohimbine; D000068438:Brimonidine Tartrate; C018564:dihydro-DIDS; D007545:Isoproterenol; D000086:Acetazolamide; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D009638:Norepinephrine; D010646:Phentolamine