Tang L Q, Hong P H, Siddiqui Y, Sarkissian E S, Huang R Y, Lee E, Krupin T
Department of Ophthalmology, Northwestern University Medical School, Chicago, IL 60611, USA.
Curr Eye Res. 1998 Jan;17(1):24-30. doi: 10.1076/ceyr.17.1.24.5258.
To study the effects of beta-adrenergic agents on intracellular potential (Vm) of the isolated and intact rabbit ciliary epithelium.
Vm was measured on the isolated intact ciliary epithelium superfused with adrenergic agents and cyclic AMP modulators.
The nonselective beta-adrenergic agonist isoproterenol depolarized Vm in a dose-dependent fashion. beta-adrenergic antagonists alone had no effect on baseline Vm. The isoproterenol response was blocked by the nonselective antagonist timolol (5 x 10(-5) M). The selective beta 2-antagonist ICI 118-551 caused a greater inhibition (IC50 approximately 7 x 10(-7)) than the selective beta 1-antagonist betaxolol (IC50 approximately 6 x 10(-6)). The isoproterenol response was also significantly (p < 0.03) blocked by the non-selective alpha-antagonist phentolamine. Cyclic AMP and phosphodiesterase inhibitors significantly decreased Vm. Pretreatment with these inhibitors potentiated the agonist-induced depolarization. Barium, a blocker of Ca(2+)-sensitive K+ channels, significantly decreased baseline Vm. Barium pretreatment blocked the beta-agonist and cAMP induced depolarization of Vm, suggesting that the K+ current is necessary for the observed isoproterenol response. Pretreatment with the cotransport inhibitor bumetanide had no effect on the isoproterenol-induced response.
The beta-adrenergic agonist isoproterenol affects ionic transport processes across the ciliary epithelium (beta 2 > beta 1). This effect is likely mediated through adenylate cyclase coupled to adrenoreceptors and requires the presence of the K+ current. Blockage of the isoproterenol-induced decrease in Vm by a nonselective alpha-adrenergic antagonist indicates an interaction between the two adrenergic systems in the ciliary epithelium.
研究β-肾上腺素能药物对离体完整兔睫状体上皮细胞内电位（Vm）的影响。
在灌注肾上腺素能药物和环磷酸腺苷调节剂的离体完整睫状体上皮细胞上测量Vm。
非选择性β-肾上腺素能激动剂异丙肾上腺素使Vm呈剂量依赖性去极化。单独使用β-肾上腺素能拮抗剂对基线Vm无影响。非选择性拮抗剂噻吗洛尔（5×10⁻⁵M）可阻断异丙肾上腺素反应。选择性β₂拮抗剂ICI 118 - 551比选择性β₁拮抗剂倍他洛尔（IC₅₀约为6×10⁻⁶）产生更大的抑制作用（IC₅₀约为7×10⁻⁷）。非选择性α-拮抗剂酚妥拉明也显著（p < 0.03）阻断了异丙肾上腺素反应。环磷酸腺苷和磷酸二酯酶抑制剂显著降低Vm。用这些抑制剂预处理可增强激动剂诱导的去极化。钡是钙敏感性钾通道的阻滞剂，可显著降低基线Vm。钡预处理可阻断β-激动剂和环磷酸腺苷诱导的Vm去极化，提示钾电流是观察到的异丙肾上腺素反应所必需的。用共转运抑制剂布美他尼预处理对异丙肾上腺素诱导的反应无影响。
β-肾上腺素能激动剂异丙肾上腺素影响跨睫状体上皮细胞的离子转运过程（β₂>β₁）。这种作用可能通过与肾上腺素受体偶联的腺苷酸环化酶介导，并且需要钾电流的存在。非选择性α-肾上腺素能拮抗剂阻断异丙肾上腺素诱导的Vm降低表明睫状体上皮细胞中两种肾上腺素能系统之间存在相互作用。
