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犬离体灌注胃网膜动脉中的嘌呤能与肾上腺素能共传递

Purinergic and adrenergic cotransmission in canine isolated and perfused gastroepiploic arteries.

作者信息

Tanaka Kenichi, Yang Xiao-Ping, Chiba Shigetoshi

机构信息

Department of Pharmacology, Shinshu University School of Medicine, Matsumoto 390-8621, Japan.

出版信息

Clin Exp Pharmacol Physiol. 2003 Sep;30(9):678-83. doi: 10.1046/j.1440-1681.2003.03897.x.

DOI:10.1046/j.1440-1681.2003.03897.x
PMID:12940888
Abstract
  1. The vasoconstrictor responses of canine gastroepiploic artery to periarterial electrical nerve stimulation (PNS; 30 s trains of pulses at a frequency of 2, 4 or 8 Hz) were observed in a frequency dependent manner. The PNS-induced vasoconstrictions were abolished by tetrodotoxin (1 micromol/L) and mostly depressed but not completely by guanethidine (10 micromol/L). 2. Vasoconstrictor responses to administered noradrenaline were antagonized significantly by prazosin (0.1 micromol/L), an alpha1-adrenoceptor antagonist, but were not significantly affected by suramin (100 micromol/L), a P2 purinoceptor antagonist, or alpha,beta-methylene ATP (1 micromol/L), a P2X receptor desensitizing agent. Exogenous ATP-induced responses were clearly depressed by suramin or alpha,beta-methylene ATP, but were not significantly affected by prazosin. 3. The vasoconstrictor responses to PNS at a low frequency (2 and 4 Hz) of stimulation were markedly inhibited by suramin (100 micromol/L) and by alpha,beta-methylene ATP (1 micromol/L). The remaining responses after suramin or alpha,beta-methylene ATP were abolished by subsequent application of prazosin (0.1 micromol/L). At a high frequency (8 Hz) of stimulation, the vascular response was not significantly inhibited by suramin or alpha,beta-methylene ATP, but it was abolished by prazosin. 4. Injection of xylazine (0.3-30 nmol/L), an alpha2-adrenoceptor agonist, did not induce any clear vasoconstriction. The exposure of tissues to rauwolscine (0.1-0.3 micromol/L), an alpha2-adrenoceptor antagonist, dose-dependently increased PNS-induced vasoconstrictions at all frequencies tested. 5. The present results indicate that ATP acts as a cotransmitter with noradrenaline and is responsible for post-junctional vasoconstrictor responses at low frequencies of sitmulation, whereas the effect of noradrenaline is dominant at high-frequency stimulation in canine gastroepiploic artery. Prejunctional alpha2-adrenoceptor autoinhibition may modulate the release of either noradrenaline or ATP from sympathetic nerve terminals.
摘要
  1. 观察到犬胃网膜动脉对动脉周围电神经刺激(PNS;频率为2、4或8 Hz的30秒脉冲串)的血管收缩反应呈频率依赖性。河豚毒素(1微摩尔/升)可消除PNS诱导的血管收缩,胍乙啶(10微摩尔/升)可使该反应大部分受到抑制但未完全消除。2. α1肾上腺素能受体拮抗剂哌唑嗪(0.1微摩尔/升)可显著拮抗对去甲肾上腺素给药的血管收缩反应,但P2嘌呤能受体拮抗剂苏拉明(100微摩尔/升)或P2X受体脱敏剂α,β-亚甲基ATP(1微摩尔/升)对此反应无显著影响。外源性ATP诱导的反应明显受到苏拉明或α,β-亚甲基ATP的抑制,但哌唑嗪对此无显著影响。3. 苏拉明(100微摩尔/升)和α,β-亚甲基ATP(1微摩尔/升)可显著抑制低频(2和4 Hz)刺激下PNS的血管收缩反应。在应用苏拉明或α,β-亚甲基ATP后剩余的反应,随后应用哌唑嗪(0.1微摩尔/升)可将其消除。在高频(8 Hz)刺激下,血管反应未受到苏拉明或α,β-亚甲基ATP的显著抑制,但可被哌唑嗪消除。4. α2肾上腺素能受体激动剂赛拉嗪(0.3 - 30纳摩尔/升)注射未诱导出明显的血管收缩。将组织暴露于α2肾上腺素能受体拮抗剂育亨宾(0.1 - 0.3微摩尔/升)下,在所有测试频率下均可剂量依赖性地增强PNS诱导的血管收缩。5. 目前的结果表明,ATP作为去甲肾上腺素的共递质,在低频刺激时负责节后血管收缩反应,而在犬胃网膜动脉高频刺激时去甲肾上腺素的作用占主导。突触前α2肾上腺素能受体自身抑制可能调节交感神经末梢去甲肾上腺素或ATP的释放。

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Neurogenic double-peaked vasoconstriction of human gastroepiploic artery is mediated by both alpha1- and alpha2-adrenoceptors.人胃网膜动脉的神经源性双峰血管收缩由α1和α2肾上腺素能受体介导。
Br J Pharmacol. 2005 Mar;144(6):737-42. doi: 10.1038/sj.bjp.0705975.