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本文引用的文献

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Adenosine receptor-induced second messenger production in adult guinea-pig cerebellum.成年豚鼠小脑中腺苷受体诱导的第二信使生成
Br J Pharmacol. 1993 Nov;110(3):1085-90. doi: 10.1111/j.1476-5381.1993.tb13925.x.
2
Adenosine receptor subtypes.腺苷受体亚型
Trends Pharmacol Sci. 1993 Oct;14(10):360-6. doi: 10.1016/0165-6147(93)90094-z.
3
Cloning and expression of the A2a adenosine receptor from guinea pig brain.豚鼠脑A2a腺苷受体的克隆与表达
Neurochem Res. 1994 May;19(5):613-21. doi: 10.1007/BF00971338.
4
A comparison of A2 adenosine receptor-induced cyclic AMP generation in cerebral cortex and relaxation of pre-contracted aorta.大脑皮层中 A2 腺苷受体诱导的环磷酸腺苷生成与预收缩主动脉舒张的比较。
Br J Pharmacol. 1994 Jan;111(1):185-90. doi: 10.1111/j.1476-5381.1994.tb14042.x.
5
Cloned adenosine A3 receptors: pharmacological properties, species differences and receptor functions.克隆的腺苷A3受体：药理学特性、种属差异及受体功能
Trends Pharmacol Sci. 1994 Aug;15(8):298-306. doi: 10.1016/0165-6147(94)90011-6.
6
Nomenclature and classification of purinoceptors.嘌呤受体的命名与分类
Pharmacol Rev. 1994 Jun;46(2):143-56.
7
A1 adenosine receptor inhibition of cyclic AMP formation and radioligand binding in the guinea-pig cerebral cortex.豚鼠大脑皮层中A1腺苷受体对环磷酸腺苷形成及放射性配体结合的抑制作用。
Br J Pharmacol. 1994 Dec;113(4):1501-7. doi: 10.1111/j.1476-5381.1994.tb17166.x.
8
Dual effect of (-)-N6-phenylisopropyl adenosine on guinea-pig trachea.(-)-N6-苯基异丙基腺苷对豚鼠气管的双重作用。
Br J Pharmacol. 1984 Sep;83(1):23-9. doi: 10.1111/j.1476-5381.1984.tb10115.x.
9
Subclasses of adenosine receptors in the central nervous system: interaction with caffeine and related methylxanthines.中枢神经系统中腺苷受体的亚类：与咖啡因及相关甲基黄嘌呤的相互作用。
Cell Mol Neurobiol. 1983 Mar;3(1):69-80. doi: 10.1007/BF00734999.
10
Evidence for an A2/Ra adenosine receptor in the guinea-pig trachea.豚鼠气管中A2/Ra腺苷受体的证据。
Br J Pharmacol. 1982 Jul;76(3):381-7. doi: 10.1111/j.1476-5381.1982.tb09231.x.

腺苷受体介导的豚鼠预收缩离体气管舒张作用。

Adenosine receptor-mediated relaxation of guinea-pig precontracted, isolated trachea.

作者信息

Losinski A, Alexander S P

机构信息

Department of Physiology & Pharmacology, University of Nottingham Medical School, Queen's Medical Centre.

出版信息

Br J Pharmacol. 1995 Nov;116(5):2425-8. doi: 10.1111/j.1476-5381.1995.tb15090.x.

DOI:10.1111/j.1476-5381.1995.tb15090.x
PMID:8581279
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1909068/
Abstract
  1. We have investigated the pharmacological profile of the adenosine receptor mediating relaxation of the carbachol pre-contracted guinea-pig trachea. 2. 5'-N-Ethylcarboxamidoadenosine (NECA) and 2-chloroadenosine elicited concentration-dependent relaxations with pD2 (-log10 half-maximal values) of 6.37 +/- 0.04 and 5.25 +/- 0.09, with maximal relaxations of 73 +/- 7 and 208 +/- 38%, respectively. In the presence of 10 microM NECA, 2-chloroadenosine was able to relax the tissue further with a pD2 value of 4.74 +/- 0.11 and a maximal response of 252 +/- 68%. 3. CGS 21680, APEC and adenosine failed to elicit significant relaxations of precontracted tracheal rings at concentrations below 10 microM. At 10 microM, adenosine analogues elicited relaxations with the following order of magnitude (% relaxation): 2-chloroadenosine (75 +/- 16%) = NECA (69 +/- 16%) > APEC (25 +/- 8%) > CGS 21680 (11 +/- 2%) > adenosine (6 +/- 4%). 4. NECA-induced relaxation of precontracted trachea was antagonized by adenosine receptor antagonists with the rank order of apparent affinity (Ki, nM): PD 115,199 (27 +/- 8) = XAC (43 +/- 11) > CP 66,713(285 +/- 89) = DPCPX (316 +/- 114). 5. We conclude that the adenosine analogue-induced relaxation of guinea-pig tracheal rings fails to fit into the current classification of A2 adenosine receptors.
摘要
  1. 我们研究了介导卡巴胆碱预收缩豚鼠气管舒张的腺苷受体的药理学特性。2. 5'-N-乙基甲酰胺基腺苷（NECA）和2-氯腺苷引起浓度依赖性舒张，其pD2（-log10半数最大值）分别为6.37±0.04和5.25±0.09，最大舒张率分别为73±7%和208±38%。在10μM NECA存在下，2-氯腺苷能够进一步舒张组织，pD2值为4.74±0.11，最大反应为252±68%。3. CGS 21680、APEC和腺苷在浓度低于10μM时未能引起预收缩气管环的显著舒张。在10μM时，腺苷类似物引起的舒张程度顺序如下（舒张百分比）：2-氯腺苷（75±16%）=NECA（69±16%）>APEC（25±8%）>CGS 21680（11±2%）>腺苷（6±4%）。4. NECA诱导的预收缩气管舒张被腺苷受体拮抗剂拮抗，其表观亲和力顺序（Ki，nM）为：PD 115,199（27±8）=XAC（43±11）>CP 66,713（285±89）=DPCPX（316±114）。5. 我们得出结论，腺苷类似物诱导的豚鼠气管环舒张不符合目前A2腺苷受体的分类。