Role of alpha 1- and alpha 2-adrenergic receptors in Cl- transport across frog corneal epithelium

Chu, Teh-Ching; Candia, Oscar A.

doi:10.1152/ajpcell.1988.255.6.c724

Cited by 25 publications

(12 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In frog corneal epithelium, short-circuit current studies showed that the Cl-transport from the aqueous to the tear side is enhanced by a,-and 13-adrenoceptor stimulation, and it is reduced by a2-adrenoceptor stimulation (6). In the present experiments, a,-adrenoceptor stimulation appeared not to affect endothelial Cl-transport.…”

Section: (7) As Shown Incontrasting

confidence: 43%

“…Transport of C1-as well as Na+ and HC03 across the corneal endothelium has been considered to be responsible for the fluid movement (2)(3)(4). In the epithelia covering the anterior surface of the cornea, Cl-transport from the stroma to tears also contributes to maintenance of corneal hydration and transparency (1,2,4), and this transport is regulated by activation of adrenergic receptors (5,6). In spite of the presence of adrenoceptors in corneal endothelia (7), the effects of adrenoceptor stimulation on Cl-transport in the endothelial cells have not been examined yet.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Adrenergic Receptor-Mediated Cl Transport in Rabbit Corneal Endothelial Cells

Yasukura

Inoue²,

Irie³

et al. 1995

Japanese Journal of Pharmacology

View full text Add to dashboard Cite

ABSTRACT-Adrenoceptor-mediated C1-transport in cultured rabbit corneal endothelium was examined using a Cl--sensitive fluorescent dye. The intracellular Cl-concentration ([C1-];) in the endothelial cells was estimated to be about 30 mM. Noradrenaline (0.001-0.1 mM) transiently decreased the [Cl-]; in a dose-dependent manner. Such a decrease in [Cl-]; was completely antagonized by pretreatment with the aadrenoceptor antagonist phentolamine (0.1 mM). The selective a2-adrenoceptor agonist UK 14304-18 (5-bromo-6-[(4H,5H-imidazol-2-yl)amino]quinoxaline, 0.1 mM) persistently decreased the [Cl-];, but neither the al-adrenoceptor agonist phenylephrine (0.1 mM) nor the ;3-adrenoceptor agonist isoproterenol (0.1 mM) had any effect. The a2-adrenoceptor agonist/antagonist yohimbine (0.1 mM) persistently and more strongly decreased the [Cl-]; than UK 14304-18 did. The yohimbine-induced decrease in the [C1-]; 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 [C1-]; 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-]; was inhibited by the Na+/K+/C1-cotransport inhibitor bumetanide (0.1 mM), but not by the Clchannel blocker 5-nitro-2-(3-phenylpropylamino)-benzoic acid. These findings suggest that corneal endothelial cells extrude Cl-upon a2-adrenoceptor stimulation and accumulate Cl-upon 13-adrenoceptor stimulation under low [C1-]; conditions, probably via acceleration of Cl-/HC03-exchange and Na+/K+/ Cl-cotransport, respectively.

show abstract

Section: (7) As Shown Incontrasting

confidence: 43%

mentioning

confidence: 99%

Adrenergic Receptor-Mediated Cl Transport in Rabbit Corneal Endothelial Cells

Yasukura

Inoue²,

Irie³

et al. 1995

Japanese Journal of Pharmacology

View full text Add to dashboard Cite

show abstract

“…In fact, it is known that the transport of chloride ions from the aqueous to the tear side, which is very important for the continuous corneal dehydration and maintenance of transparency, is under adrenergic control [15,17,18,42]. The description of corneal opacities and edemas by many adrenergic agents support this hypothesis [22,43,44].…”

Section: Discussionmentioning

confidence: 99%

“…In 1990 [11], following the description of the dramatic effect of XYL/KET on the aqueous concentration of glucose [12], the opacification of the lens was recognized as a typical sugar cataract [13,14], suggesting that an osmotic mechanism could also be responsible for corneal decompensation and transient loss of transparency. However, other mechanistic hypotheses cannot be ruled out, including the perturbation of the adrenergic control of corneal hydration and transparency [15][16][17][18] as indicated by the known corneal toxicity of other ·-agonists [19][20][21][22][23]. Corneal toxic effects of clonidine (CLO), another selective · 2 -adrenergic agonist, have been described in the rat [24], but not in humans, despite its wide use as a systemic hypotensive drug and anesthetic adjuvant [25][26][27].…”

Section: Introductionmentioning

confidence: 99%

Corneal Toxicity of Xylazine and Clonidine, in Combination with Ketamine, in the Rat

et al. 2001

View full text Add to dashboard Cite

Purpose: To compare the corneal toxicity of xylazine (XYL)/ketamine (KET) with that of clonidine (CLO)/KET in the rat, in the presence or not of the α₂-adrenergic antagonist yohimbine (YOH). Methods: XYL (10 mg/kg) and CLO (0.15 mg/kg) were administered subcutaneously in the rat in combination with KET (50 mg/kg), in the presence or not of YOH (2 mg/kg). Results: The corneas immediately lost transparency and luster, but recovered within 120 min. By both light and electron microscopy, a marked stromal edema and alterations of all layers were observed. In addition, XYL/KET altered the permeability of the cornea as indicated by the augmented levels of ¹⁴C-indomethacin, topically administered 30 min after the anesthetic combination. Conclusions: The mechanism of the corneal toxicity of XYL and CLO in the rat is unclear but we speculate that: (a) proptosis and inhibition of normal blinking did not play a major role because topical application of hyaluronic acid did not protect against it; corneal decompensation, edema and opacification could be due to (b) osmotic or (c) mechanical endothelial stress: the first resulting from the sudden increase of the glucose concentration in the aqueous humor due to the well-known inhibition of insulin release by α₂-adrenergic agonists, and the second from the acute elevation of intraocular pressure caused by these α₂-adrenergic mydriatics in the rat; (d) addition, XYL and CLO could act by directly interacting with local α₂- or, possibly, α₁-adrenergic receptors, whose function is still not clear but probably essential for corneal homeostasis.

show abstract

“…Functional studies demonstrated ␣ 2 -adrenoceptor activity in frog corneal epithelium [12] . Corneal epithelial ␤ -adrenoceptors have been associated with stimulation of adenylyl cyclase and cAMP-dependent protein kinase [13] .…”

Section: Pka In Corneal Epithelium and Endotheliummentioning

confidence: 99%

Adrenergic Regulation of cAMP/Protein Kinase A Pathway in Corneal Epithelium and Endothelium

2008

View full text Add to dashboard Cite

Purpose: The G-protein-coupled receptor/cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) pathway is one of the most common and versatile signal pathways in eukaryotic cells. The aim of this study was to characterize subtypes of adrenergic G-protein-coupled receptors and their influence on cAMP concentration and PKA activity in bovine corneal epithelial and endothelial cells. Procedures: Adrenergic receptors and PKA were studied using polyclonal antibodies. cAMP concentration was determined with an enzyme immunoassay, and PKA activity was estimated by the kinases consumption of adenosine triphosphate. Results: In bovine corneal epithelial and endothelial cells, immunocytochemistry and Western blot were positive for α₁-, α_2A-, β₁- and β₂-adrenergic receptors. Stimulation of corneal epithelial and endothelial β-adrenoceptors with isoprenaline led to a dose-dependent increase in cAMP concentration and activation of PKA. Stimulation of corneal α_2A-adrenoceptors with brimonidine resulted in a dose-dependent decrease in cAMP concentration and the inhibition of PKA activity. Conclusions: In corneal epithelial and endothelial cells, β-adrenergic stimulation leads to activation of PKA via stimulation of adenylyl cyclase, and α_2A-adrenoceptor stimulation inhibits PKA activity via inhibition of adenylyl cyclase. Stimulation and inhibition of the corneal cAMP-PKA pathway may play a role in important corneal functions such as wound healing or homeostasis. Long-term therapy with α_2A-agonists or β-antagonists may influence these functions in a currently unknown way.

show abstract

Role of alpha 1- and alpha 2-adrenergic receptors in Cl- transport across frog corneal epithelium

Cited by 25 publications

References 17 publications

Adrenergic Receptor-Mediated Cl Transport in Rabbit Corneal Endothelial Cells

Adrenergic Receptor-Mediated Cl Transport in Rabbit Corneal Endothelial Cells

Corneal Toxicity of Xylazine and Clonidine, in Combination with Ketamine, in the Rat

Adrenergic Regulation of cAMP/Protein Kinase A Pathway in Corneal Epithelium and Endothelium

Contact Info

Product

Resources

About