通过强直性A2a - 腺苷受体激活增强降钙素基因相关肽促进大鼠运动神经末梢释放[3H] - 乙酰胆碱的作用。
Potentiation by tonic A2a-adenosine receptor activation of CGRP-facilitated [3H]-ACh release from rat motor nerve endings.
作者信息
Correia-de-Sá P, Ribeiro J A
机构信息
Laboratory of Pharmacology, ICBAS, University of Oporto, Portugal.
出版信息
Br J Pharmacol. 1994 Feb;111(2):582-8. doi: 10.1111/j.1476-5381.1994.tb14777.x.
Abstract
- The effect of calcitonin gene-related peptide (CGRP) on [3H]-acetylcholine ([3H]-ACh) release from motor nerve endings and its interaction with presynaptic facilitatory A2a-adenosine and nicotinic acetylcholine receptors was studied on rat phrenic nerve-hemidiaphragm preparations loaded with [3H]-choline. 2. CGRP (100-400 nM) increased electrically evoked [3H]-ACh release from phrenic nerve endings in a concentration-dependent manner. 3. The magnitude of CGRP excitation increased with the increase of the stimulation pulse duration from 40 microseconds to 1 ms, keeping the frequency, the amplitude and the train length constants. With 1 ms pulses, the evoked [3H]-ACh release was more intense than with 40 microseconds pulse duration. 4. Both the nicotinic acetylcholine receptor agonist, 1,1-dimethyl-4-phenylpiperazinium, and the A2a adenosine receptor agonist, CGS 21680C, increased evoked [3H]-ACh release, but only CGS 21680C potentiated the facilitatory effect of CGRP. This potentiation was prevented by the A2a adenosine receptor antagonist, PD 115,199. 5. Adenosine deaminase prevented the excitatory effect of CGRP (400 nM) on [3H]-ACh release. This effect was reversed by the non-hydrolysable A2a-adenosine receptor agonist, CGS 21680C. 6. The nicotinic antagonist, tubocurarine, did not significantly change, whereas the A2-adenosine receptor antagonist, PD 115,199, blocked the CGRP facilitation. The A1-adenosine receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine, potentiated the CGRP excitatory effect. 7. The results suggest that the facilitatory effect of CGRP on evoked [3H]-ACh release from rat phrenic motor nerve endings depends on the presence of endogenous adenosine which tonically activates A2a-adenosine receptors. Since both CGRP and A2a-adenosine receptors are positively coupled to the adenylate cyclase/cyclic AMP system, cooperation between these receptors might occur at the second messenger transduction system level.
摘要
- 研究了降钙素基因相关肽（CGRP）对[3H] - 乙酰胆碱（[3H] - ACh）从运动神经末梢释放的影响，以及它与突触前易化性A2a - 腺苷和烟碱型乙酰胆碱受体的相互作用，实验采用负载[3H] - 胆碱的大鼠膈神经 - 半膈肌标本。2. CGRP（100 - 400 nM）以浓度依赖性方式增加膈神经末梢电诱发的[3H] - ACh释放。3. 当刺激脉冲持续时间从40微秒增加到1毫秒，频率、幅度和串长保持恒定时，CGRP的兴奋幅度增加。使用1毫秒脉冲时，诱发的[3H] - ACh释放比40微秒脉冲持续时间时更强烈。4. 烟碱型乙酰胆碱受体激动剂1,1 - 二甲基 - 4 - 苯基哌嗪鎓和A2a腺苷受体激动剂CGS 21680C均增加诱发的[3H] - ACh释放，但只有CGS 21680C增强了CGRP的易化作用。A2a腺苷受体拮抗剂PD 115,199可阻止这种增强作用。5. 腺苷脱氨酶可阻止CGRP（400 nM）对[3H] - ACh释放的兴奋作用。不可水解的A2a - 腺苷受体激动剂CGS 21680C可逆转这种作用。6. 烟碱拮抗剂筒箭毒碱无显著变化，而A2 - 腺苷受体拮抗剂PD 115,199可阻断CGRP的易化作用。A1 - 腺苷受体拮抗剂1,3 - 二丙基 - 8 - 环戊基黄嘌呤增强了CGRP的兴奋作用。7. 结果表明，CGRP对大鼠膈运动神经末梢诱发的[3H] - ACh释放的易化作用取决于内源性腺苷的存在，内源性腺苷可持续性激活A2a - 腺苷受体。由于CGRP和A2a - 腺苷受体均与腺苷酸环化酶/环磷酸腺苷系统正性偶联，这些受体之间可能在第二信使转导系统水平发生协同作用。
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