Bausher L P, Gregory D S, Sears M L
Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, CT 06510.
Curr Eye Res. 1989 Jan;8(1):47-54. doi: 10.3109/02713688909013893.
The interaction between alpha 2-adrenergic and VIP receptors has been studied by examining inhibition of VIP-stimulated cyclic AMP production by adrenergic agonists in intact, excised rabbit ciliary processes. Epinephrine, norepinephrine, isoproterenol, dopamine, and the specific alpha 2-adrenergic agonists clonidine and p-aminoclonidine exhibit dose-dependent inhibition of VIP-stimulated cyclic AMP production. I50s, clonidine (0.05 microM) = p-aminoclonidine (0.05 microM) congruent to epinephrine (0.1 microM) less than norepinephrine (2.0 microM) less than isoproterenol (15 microM) = dopamine (15 microM), are consistent with the characteristic binding affinities of these adrenergic agonists for alpha 2-adrenergic receptors. Inhibition of VIP-stimulated cyclic AMP production by clonidine, epinephrine, isoproterenol, and dopamine is blocked by yohimbine but not by prazosin. These data establish the alpha 2-adrenergic specificity of the inhibitory effects observed. We have previously shown that beta 2-adrenergic receptor-mediated stimulation of cyclic AMP production in rabbit ciliary processes is also inhibited by postjunctional alpha 2-adrenergic receptors. These studies support the idea that the catecholamines may regulate aqueous humor formation by inhibiting stimulation of cyclic AMP production via postjunctional alpha 2-adrenergic receptors in ciliary processes.
通过检测肾上腺素能激动剂对完整的、离体兔睫状体中血管活性肠肽(VIP)刺激的环磷酸腺苷(cAMP)生成的抑制作用,研究了α2 - 肾上腺素能受体与VIP受体之间的相互作用。肾上腺素、去甲肾上腺素、异丙肾上腺素、多巴胺以及特异性α2 - 肾上腺素能激动剂可乐定和对氨基可乐定均表现出对VIP刺激的cAMP生成的剂量依赖性抑制作用。半数抑制浓度(I50s),可乐定(0.05微摩尔/升)=对氨基可乐定(0.05微摩尔/升)≈肾上腺素(0.1微摩尔/升)<去甲肾上腺素(2.0微摩尔/升)<异丙肾上腺素(15微摩尔/升)=多巴胺(15微摩尔/升),与这些肾上腺素能激动剂对α2 - 肾上腺素能受体的特征性结合亲和力一致。可乐定、肾上腺素、异丙肾上腺素和多巴胺对VIP刺激的cAMP生成的抑制作用可被育亨宾阻断,但不能被哌唑嗪阻断。这些数据证实了所观察到的抑制作用具有α2 - 肾上腺素能特异性。我们之前已经表明,兔睫状体中环磷酸腺苷生成的β2 - 肾上腺素能受体介导的刺激作用也受到节后α2 - 肾上腺素能受体的抑制。这些研究支持这样一种观点,即儿茶酚胺可能通过抑制睫状体节后α2 - 肾上腺素能受体对环磷酸腺苷生成的刺激来调节房水生成。