首页> 美国卫生研究院文献>British Journal of Pharmacology and Chemotherapy >Contributions of alpha 1-adrenoceptors alpha 2-adrenoceptors and P2x-purinoceptors to neurotransmission in several rabbit isolated blood vessels: role of neuronal uptake and autofeedback.
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Contributions of alpha 1-adrenoceptors alpha 2-adrenoceptors and P2x-purinoceptors to neurotransmission in several rabbit isolated blood vessels: role of neuronal uptake and autofeedback.

机译:α1肾上腺素受体α2肾上腺素受体和P2x嘌呤受体对几种兔离体血管中神经传递的贡献:神经元摄取和自动反馈的作用。

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摘要

1. The roles of autofeedback and neuronal uptake in neurotransmission produced by electrical field stimulation in several rabbit isolated blood vessels were examined. 2. Blocking drugs were used to separate the possible purinergic and noradrenergic contributions to the end organ response: prazosin, antagonist at postjunctional alpha 1-adrenoceptors; rauwolscine and yohimbine, antagonists at pre- and postjunctional alpha 2-adrenoceptors; alpha,beta-methylene ATP, desensitizing agent at postjunctional P2x-purinoceptors. In addition to desensitizing postjunctional P2x-purinoceptors, alpha,beta-methylene ATP potentiated the noradrenergic component of the nerve-induced responses. 3. In the presence of an intact neuronal uptake mechanism, the vessels showed different contributions of purinergic (via P2x-purinoceptors) and noradrenergic (via alpha 1-adrenoceptors and alpha 2-adrenoceptors) components to the end organ response to nerve stimulation: saphenous artery (approximately equal contributions from P2x-purinoceptors and alpha 1-adrenoceptors), ileocolic artery (mainly P2x-purinoceptors with a smaller contribution from alpha 1-adrenoceptors), plantaris vein (mainly alpha 1-adrenoceptors with a small contribution from alpha 2-adrenoceptors and P2x-purinoceptors) and saphenous vein (alpha 1-adrenoceptors). 4. The presence of alpha 2-adrenoceptor-mediated autofeedback could be demonstrated for both purinergic and noradrenergic components of the nerve-induced responses in the artery preparations. In the veins, potentiation of nerve-induced responses by alpha 2-adrenoceptor antagonists could not be studied due to blockade of postjunctional alpha 2-adrenoceptor-mediated vasoconstriction. 5. Blockade of neuronal uptake with cocaine potentiated the noradrenergic component of the nerve-induced responses.(ABSTRACT TRUNCATED AT 250 WORDS)
机译:1.考察了自反馈和神经元摄取在电场刺激下在几只兔离体血管中产生的神经传递中的作用。 2.阻断药被用于分离可能的嘌呤能和去甲肾上腺素能对终末期器官反应的贡献:哌唑嗪,结后α1-肾上腺素受体拮抗剂。 rauwolscine和育亨宾,结前和结后α2-肾上腺素受体的拮抗剂; α,β-亚甲基ATP,连接后P2x-嘌呤受体的脱敏剂。除了使连接后的P2x嘌呤受体脱敏外,α,β-亚甲基ATP还增强了神经诱发反应的去甲肾上腺素成分。 3.在存在完整的神经元摄取机制的情况下,血管显示嘌呤能(通过P2x-嘌呤受体)和去甲肾上腺素(通过α1-肾上腺素受体和α2-肾上腺素受体)成分对终末器官对神经刺激的反应有不同的贡献:隐性动脉(P2x-嘌呤受体和α1-肾上腺素受体的贡献大致相等),回肠动脉(主要是P2x-嘌呤受体,其中α1-肾上腺素受体的贡献较小),plant静脉(主要是α1-肾上腺素受体,α2-肾上腺素的贡献较小肾上腺素受体和P2x嘌呤受体)和隐静脉(α1肾上腺素受体)。 4.对于动脉制剂中神经诱发反应的嘌呤能和去甲肾上腺素能成分,都可以证明存在α2-肾上腺素受体介导的自动反馈。在静脉中,由于α2肾上腺素受体介导的血管收缩的阻滞作用,因此无法研究α2肾上腺素受体拮抗剂对神经诱导反应的增强作用。 5.用可卡因阻断神经元摄取增强了神经诱发反应的去甲肾上腺素能成分。(摘要截短为250字)

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