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首页> 外文OA文献 >The possible role of ATP and PACAP as mediators of apaminsensitive NANC inhibitory junction potentials in circular muscle of guinea-pig colon.
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The possible role of ATP and PACAP as mediators of apaminsensitive NANC inhibitory junction potentials in circular muscle of guinea-pig colon.

机译：ATP和PACAP作为豚鼠结肠环形肌中对氨纶敏感的NANC抑制性连接电位的介质的可能作用。

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1. In the presence of atropine (1 microM), guanethidine (3 microM), indomethacin (3 microM), nifedipine (1 microM), L-nitroarginine (L-NOARG, 100 microM), and the selective tachykinin NK1 and NK2 receptor antagonists, SR 140,333 and GR 94,800, respectively (0.1 microM each), a single pulse of electrical field stimulation (EFS) produced a monophasic non-adrenergic non-cholinergic (NANC) inhibitory junction potential (i.j.p., about 10 mV in amplitude) in the circular muscle of guinea-pig proximal colon, recorded by the modified single sucrose gap technique. 2. The P2 purinoceptor agonist, alpha, beta methylene ATP (alpha, beta mATP, 100 microM) and the pituitary adenylyl cyclase activating peptide (PACAP, 1 microM) both produced hyperpolarization (11 +/- 0.8 mV, n = 14 and 10.2 +/- 0.8 mV, n = 19, respectively) and relaxation (1.1 +/- 0.2 mV, n = 14 and 1.5 +/- 0.2 mN, n = 19, respectively) of the circular muscle. 3. Apamin (0.1 microM) nearly abolished (about 90% inhibition) the NANC i.j.p. and the alpha, beta mATP-induced hyperpolarization, markedly reduced the alpha, beta mATP-induced relaxation (73% inhibition) and the PACAP-induced hyperpolarization (65% inhibition), while the PACAP-induced relaxation was unaffected. 4. Tetraethylammonium (TEA, 10 mM) increased the EFS-evoked i.j.p. and revealed an excitatory junction potential (e.j.p.). In the presence of TEA, alpha, beta mATP induced a biphasic response: transient depolarization and contraction followed by hyperpolarization and relaxation. The hyperpolarization to PACAP was reduced by TEA (45% inhibition) but the relaxation was unaffected. 5. The combined application of apamin (0.1 microM) and TEA (10 mM) abolished the i.j.p. and single pulse EFS evoked a pure e.j.p. with latency three times longer than that of the i.j.p. In the majority of strips tested, alpha, beta mATP and PACAP elicited a biphasic response : depolarization and small contraction followed by hyperpolarization and relaxation. 6. The P2 purinoceptor antagonist, pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) inhibited the NANC i.j.p. in concentration-dependent manner and inhibited the alpha, beta mATP-induced hyperpolarization and relaxation, without affecting the hyperpolarization and relaxation induced by PACAP. On the other hand, the P2 purinoceptor antagonist, suramin (100 microM) inhibited to a similar extent (60-80%) the NANC i.j.p. and the hyperpolarization and relaxation induced by alpha, beta mATP or PACAP. 7. PPADS and suramin reduced the NANC e.j.p. evoked by a single pulse EFS in the presence of apamin and TEA (100 microM of PPADS and 300 microM of suramin inhibited the e.j.p. by about 40%). 8. We conclude that ATP, but not PACAP, mediates the apamin-sensitive NANC i.j.p. in the circular muscle of the guinea-pig colon. After blockade of the NANC i.j.p., ATP may act as an excitatory transmitter by activating excitatory P2 purinoceptors. The subtypes of P2 purinoceptor involved in the inhibitory and excitatory responses remain to be established. The data suggest that excitatory P2 purinoceptors may be located extrajunctionally.
机译：1.在存在阿托品（1 microM），胍乙啶（3 microM），消炎痛（3 microM），硝苯地平（1 microM），L-硝基精氨酸（L-NOARG，100 microM）和选择性速激肽NK1和NK2受体存在下分别是SR 140,333和GR 94,800拮抗剂（各自为0.1 microM），电场的单个脉冲（EFS）产生了单相非肾上腺素非胆碱能（NANC）抑制性连接电位（ijp，振幅约10 mV）。用改良的单蔗糖间隙技术记录豚鼠近端结肠的环形肌。 2. P2嘌呤受体激动剂，α，β亚甲基ATP（α，βmATP，100 microM）和垂体腺苷酸环化酶激活肽（PACAP，1 microM）均产生超极化作用（11 +/- 0.8 mV，n = 14和10.2）。 +/- 0.8 mV，n = 19）和松弛（1.1 +/- 0.2 mV，n = 14和1.5 +/- 0.2 mN，n = 19）。 3. Apamin（0.1 microM）几乎废除了（约90％抑制）NANCi.j.p。 α，βmATP诱导的超极化明显降低了α，βmATP诱导的松弛（抑制73％）和PACAP诱导的超极化（抑制65％），而PACAP诱导的松弛不受影响。 4.四乙铵（TEA，10 mM）增加了EFS诱发的i.j.p。并显示出兴奋性连接电位（e.j.p.）。在TEA的存在下，α，βmATP会诱导双相反应：短暂的去极化和收缩，然后是超极化和松弛。 TEA减少了PACAP的超极化作用（抑制了45％），但弛豫不受影响。 5. apamin（0.1 microM）和TEA（10 mM）的联合应用废除了i.j.p.。单脉冲EFS引起纯e.j.p.延迟时间是i.j.p.的三倍在大多数测试条中，α，βmATP和PACAP引起双相反应：去极化和小收缩，然后超极化和松弛。 6.P2嘌呤受体拮抗剂吡pyr草磷酸-6-偶氮苯基-2′，4′-二磺酸（PPADS）抑制了NANCi.j.p。以浓度依赖性方式抑制α，βmATP诱导的超极化和松弛，而不影响PACAP诱导的超极化和松弛。另一方面，P2嘌呤受体拮抗剂苏拉明（100 microM）对NANC i.j.p.的抑制程度相似（60-80％）。以及由α，βmATP或PACAP引起的超极化和松弛。 7. PPADS和苏拉明降低了NANC e.j.p.在存在apapamin和TEA的情况下由单脉冲EFS引起（100 microM PPADS和300 microM suramin抑制e.j.p.约40％）。 8.我们得出的结论是，ATP，而不是PACAP，介导对apapamin敏感的NANCi.j.p。在豚鼠结肠的环形肌肉中。阻断NANC i.j.p.后，ATP可以通过激活兴奋性P2嘌呤受体来充当兴奋性递质。参与抑制和兴奋反应的P2嘌呤受体亚型仍有待建立。数据表明，兴奋性P2嘌呤受体可能位于结外。

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