A1 腺苷受体在介导腺苷诱导的大鼠膈膜小动脉血管舒张中的主要作用：一氧化氮和 ATP 依赖性钾通道的参与

Predominant role of A1 adenosine receptors in mediating adenosine induced vasodilatation of rat diaphragmatic arterioles: involvement of nitric oxide and the ATP-dependent K+ channels.

作者信息

Danialou G, Vicaut E, Sambe A, Aubier M, Boczkowski J

机构信息

INSERM U408, Faculté Xavier Bichat, Paris, France.

出版信息

Br J Pharmacol. 1997 Aug;121(7):1355-63. doi: 10.1038/sj.bjp.0701247.

DOI:10.1038/sj.bjp.0701247

PMID:9257914

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1564813/

Abstract

We investigated, by intravital microscopy in rats, the role of the subtypes of adenosine receptors A1 (A1/AR) and A2 (A2AR) in mediating adenosine-induced vasodilatation of second and third order arterioles of the diaphragm. 2. Adenosine, and the A1AR selective agonists R(-)-N6-(2-phenylisopropyl)-adenosine (R-PIA) and N6-cyclo-pentyl-adenosine (CPA) induced a similar concentration-dependent dilatation of diaphragmatic arterioles. The non selective A2AR subtype agonist N6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl) ethyl]adenosine (DPMA) also dilated diaphragmatic arterioles but induced a significantly smaller dilatation than adenosine. By contrast the selective A(2a)AR subtype agonist 2-[p-(2-carboxyethyl)phenyl amino]-5'-N-ethyl carboxamido adenosine (CGS 21680) did not modify diaphragmatic arteriolar diameter. 3. The non selective adenosine receptor antagonist 1,3-dipropyl-8-p-sulphophenylxanthine (SPX, 100 microM) and the selective A1AR antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX, 50 nM) significantly attenuated adenosine-induced dilatation of diaphragmatic arterioles. By contrast, adenosine significantly dilated diaphragmatic arterioles in the presence of A2AR antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 10 microM). 4. The dilatation induced by adenosine was unchanged by the mast cell stabilizing agent sodium cromoglycate (cromolyn, 10 microM). 5. The nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine (L-NOARG, 300 microM) attenuated the dilatation induced by adenosine, and by the A1AR and A2AR agonists. 6. The ATP-dependent K+ channel blocker glibenclamide (3 microM) significantly attenuated diaphragmatic arteriolar dilatation induced by adenosine and by the A1AR agonists R-PIA and CPA. By contrast, glibenclamide did not significantly modify arteriolar dilatation induced by the A2AR agonist DPMA. 7. These findings suggest that adenosine-induced dilatation of diaphragmatic arterioles in the rat is predominantly mediated by the A1AR, via the release of NO and activation of the ATP-dependent K+ channels.

摘要

我们通过对大鼠进行活体显微镜检查，研究了腺苷受体A1（A1/AR）和A2（A2AR）亚型在介导腺苷诱导的膈肌二级和三级小动脉血管舒张中的作用。2. 腺苷以及A1AR选择性激动剂R(-)-N6-(2-苯异丙基)-腺苷（R-PIA）和N6-环戊基-腺苷（CPA）诱导膈肌小动脉产生类似的浓度依赖性舒张。非选择性A2AR亚型激动剂N6-[2-(3,5-二甲氧基苯基)-2-(2-甲基苯基)乙基]腺苷（DPMA）也使膈肌小动脉舒张，但诱导的舒张程度明显小于腺苷。相比之下，选择性A(2a)AR亚型激动剂2-[对-(2-羧乙基)苯基氨基]-5'-N-乙基羧酰胺腺苷（CGS 21680）未改变膈肌小动脉直径。3. 非选择性腺苷受体拮抗剂1,3-二丙基-8-对磺基苯基黄嘌呤（SPX，100 microM）和选择性A1AR拮抗剂8-环戊基-1,3-二丙基黄嘌呤（CPX，50 nM）显著减弱腺苷诱导的膈肌小动脉舒张。相比之下，在A2AR拮抗剂3,7-二甲基-1-炔丙基黄嘌呤（DMPX，10 microM）存在的情况下，腺苷使膈肌小动脉显著舒张。4. 肥大细胞稳定剂色甘酸钠（色甘酸，10 microM）不改变腺苷诱导的舒张。5. 一氧化氮（NO）合酶抑制剂Nω-硝基-L-精氨酸（L-NOARG，300 microM）减弱腺苷以及A1AR和A2AR激动剂诱导的舒张。6. ATP依赖性钾通道阻滞剂格列本脲（3 microM）显著减弱腺苷以及A1AR激动剂R-PIA和CPA诱导的膈肌小动脉舒张。相比之下，格列本脲未显著改变A2AR激动剂DPMA诱导的小动脉舒张。7. 这些发现表明，大鼠中腺苷诱导的膈肌小动脉舒张主要由A1AR介导，通过释放NO和激活ATP依赖性钾通道实现。

相似文献

Predominant role of A1 adenosine receptors in mediating adenosine induced vasodilatation of rat diaphragmatic arterioles: involvement of nitric oxide and the ATP-dependent K+ channels.A1 腺苷受体在介导腺苷诱导的大鼠膈膜小动脉血管舒张中的主要作用：一氧化氮和 ATP 依赖性钾通道的参与

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A1 and A2 adenosine receptor modulation of contractility in the cauda epididymis of the guinea-pig.豚鼠附睾尾部收缩性的 A1 和 A2 腺苷受体调节

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Adenosine mediates relaxation of human small resistance-like coronary arteries via A2B receptors.腺苷通过A2B受体介导人类小阻力样冠状动脉的舒张。

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A1 腺苷受体在介导腺苷诱导的大鼠膈膜小动脉血管舒张中的主要作用：一氧化氮和 ATP 依赖性钾通道的参与

Predominant role of A1 adenosine receptors in mediating adenosine induced vasodilatation of rat diaphragmatic arterioles: involvement of nitric oxide and the ATP-dependent K+ channels.

作者信息

Danialou G, Vicaut E, Sambe A, Aubier M, Boczkowski J

机构信息

INSERM U408, Faculté Xavier Bichat, Paris, France.

出版信息

Br J Pharmacol. 1997 Aug;121(7):1355-63. doi: 10.1038/sj.bjp.0701247.

DOI:10.1038/sj.bjp.0701247

PMID:9257914

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1564813/

Abstract

We investigated, by intravital microscopy in rats, the role of the subtypes of adenosine receptors A1 (A1/AR) and A2 (A2AR) in mediating adenosine-induced vasodilatation of second and third order arterioles of the diaphragm. 2. Adenosine, and the A1AR selective agonists R(-)-N6-(2-phenylisopropyl)-adenosine (R-PIA) and N6-cyclo-pentyl-adenosine (CPA) induced a similar concentration-dependent dilatation of diaphragmatic arterioles. The non selective A2AR subtype agonist N6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl) ethyl]adenosine (DPMA) also dilated diaphragmatic arterioles but induced a significantly smaller dilatation than adenosine. By contrast the selective A(2a)AR subtype agonist 2-[p-(2-carboxyethyl)phenyl amino]-5'-N-ethyl carboxamido adenosine (CGS 21680) did not modify diaphragmatic arteriolar diameter. 3. The non selective adenosine receptor antagonist 1,3-dipropyl-8-p-sulphophenylxanthine (SPX, 100 microM) and the selective A1AR antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX, 50 nM) significantly attenuated adenosine-induced dilatation of diaphragmatic arterioles. By contrast, adenosine significantly dilated diaphragmatic arterioles in the presence of A2AR antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 10 microM). 4. The dilatation induced by adenosine was unchanged by the mast cell stabilizing agent sodium cromoglycate (cromolyn, 10 microM). 5. The nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine (L-NOARG, 300 microM) attenuated the dilatation induced by adenosine, and by the A1AR and A2AR agonists. 6. The ATP-dependent K+ channel blocker glibenclamide (3 microM) significantly attenuated diaphragmatic arteriolar dilatation induced by adenosine and by the A1AR agonists R-PIA and CPA. By contrast, glibenclamide did not significantly modify arteriolar dilatation induced by the A2AR agonist DPMA. 7. These findings suggest that adenosine-induced dilatation of diaphragmatic arterioles in the rat is predominantly mediated by the A1AR, via the release of NO and activation of the ATP-dependent K+ channels.

摘要

我们通过对大鼠进行活体显微镜检查，研究了腺苷受体A1（A1/AR）和A2（A2AR）亚型在介导腺苷诱导的膈肌二级和三级小动脉血管舒张中的作用。2. 腺苷以及A1AR选择性激动剂R(-)-N6-(2-苯异丙基)-腺苷（R-PIA）和N6-环戊基-腺苷（CPA）诱导膈肌小动脉产生类似的浓度依赖性舒张。非选择性A2AR亚型激动剂N6-[2-(3,5-二甲氧基苯基)-2-(2-甲基苯基)乙基]腺苷（DPMA）也使膈肌小动脉舒张，但诱导的舒张程度明显小于腺苷。相比之下，选择性A(2a)AR亚型激动剂2-[对-(2-羧乙基)苯基氨基]-5'-N-乙基羧酰胺腺苷（CGS 21680）未改变膈肌小动脉直径。3. 非选择性腺苷受体拮抗剂1,3-二丙基-8-对磺基苯基黄嘌呤（SPX，100 microM）和选择性A1AR拮抗剂8-环戊基-1,3-二丙基黄嘌呤（CPX，50 nM）显著减弱腺苷诱导的膈肌小动脉舒张。相比之下，在A2AR拮抗剂3,7-二甲基-1-炔丙基黄嘌呤（DMPX，10 microM）存在的情况下，腺苷使膈肌小动脉显著舒张。4. 肥大细胞稳定剂色甘酸钠（色甘酸，10 microM）不改变腺苷诱导的舒张。5. 一氧化氮（NO）合酶抑制剂Nω-硝基-L-精氨酸（L-NOARG，300 microM）减弱腺苷以及A1AR和A2AR激动剂诱导的舒张。6. ATP依赖性钾通道阻滞剂格列本脲（3 microM）显著减弱腺苷以及A1AR激动剂R-PIA和CPA诱导的膈肌小动脉舒张。相比之下，格列本脲未显著改变A2AR激动剂DPMA诱导的小动脉舒张。7. 这些发现表明，大鼠中腺苷诱导的膈肌小动脉舒张主要由A1AR介导，通过释放NO和激活ATP依赖性钾通道实现。

A1 腺苷受体在介导腺苷诱导的大鼠膈膜小动脉血管舒张中的主要作用：一氧化氮和 ATP 依赖性钾通道的参与

Predominant role of A1 adenosine receptors in mediating adenosine induced vasodilatation of rat diaphragmatic arterioles: involvement of nitric oxide and the ATP-dependent K+ channels.

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A1 腺苷受体在介导腺苷诱导的大鼠膈膜小动脉血管舒张中的主要作用：一氧化氮和 ATP 依赖性钾通道的参与

Predominant role of A1 adenosine receptors in mediating adenosine induced vasodilatation of rat diaphragmatic arterioles: involvement of nitric oxide and the ATP-dependent K+ channels.

作者信息

机构信息

出版信息