Synergistic increase in Ca2+ produced by A(1) adenosine and muscarinic receptor activation via a pertussis-toxin-sensitive pathway in epithelial cells of the rabbit ciliary body
Synergistic increase in Ca2+ produced by A(1) adenosine and muscarinic receptor activation via a pertussis-toxin-sensitive pathway in epithelial cells of the rabbit ciliary body
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DOI：
10.1006/exer.1996.0194
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发表时间：
1997-02-01
影响因子：
3.4
通讯作者：
Cilluffo, MC
中科院分区：
文献类型：
--
作者：
Farahbakhsh, NA;Cilluffo, MC
采用fura-2荧光比成像技术研究了腺苷和乙酰胆碱对兔纤毛体非色素上皮细胞胞内游离ca2 +浓度的联合影响。乙酰胆碱（10 μ M）本身产生[Ca2+]适度增加(i)。乙酰胆碱与腺苷或与A(1)特异性激动剂n -6-环己基腺苷、n -6-环戊基腺苷和(R)- n -6-（2-苯基-1-甲基乙基）-腺苷（0.1-1 μ M）联合使用时，可诱导[Ca2+](i)大量增加，而A(1)特异性拮抗剂8-环戊基-1,3-二丙基黄嘌呤可阻断这种增加。然而，A(2)特异性激动剂2-[（p-2-羧基乙基）-苯乙胺]-5'- n -乙基羧基腺苷和拮抗剂3,7-二甲基-1-（2-丙基）黄嘌呤没有效果。与百日咳毒素孵育的组织没有改变对ACh单独的反应，但消除了腺苷（或肾上腺素）的协同作用。结论是，在兔纤毛体上皮细胞中，腺苷和肾上腺素协同增强了ACh产生的[Ca2+](i)的增加。这种增强似乎是通过百日咳-毒素敏感途径发生的，可能是通过G(i)。(C) 1997学术出版社有限公司
The combined effects of adenosine and acetylcholine on the intracellular free-Ca2+ concentration in nonpigmented epithelial cells of the rabbit ciliary body were investigated using fura-2 fluorescence-ratio imaging. Acetylcholine (10 mu M) by itself produced a modest increase in [Ca2+](i). Acetylcholine in combination with adenosine, or with the A(1)-specific agonists N-6-cyclohexyl-adenosine, N-6-cyclopentyladenosine and (R)-N-6-(2-phenyl-1-methylethyl)-adenosine (0.1-1 mu M), induced a massive increase in [Ca2+](i), which could be blocked by the A(1)-specific antagonist 8-cyclopentyl-1,3-dipropylxanthine. However, the A(2)-specific agonist 2-[(p-2-carboxyethyl)-phenethylamino]-5'-N-ethylcarboxamide-adenosine and the antagonist 3,7-dimethyl-1-(2-propynyl)xanthine were without effect. Incubation of the tissue with pertussis toxin did not alter the response to ACh alone but eliminated the synergistic effect of adenosine (or of epinephrine), It was concluded that in the epithelial cells of the rabbit ciliary body, adenosine and epinephrine synergistically potentiate the rise in [Ca2+](i) produced by ACh. This potentiation appears to occur via a pertussis-toxin-sensitive pathway, perhaps through G(i). (C) 1997 Academic Press Limited.