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1
Stimulation of cyclic GMP production in cultured endothelial cells of the pig by bradykinin, adenosine diphosphate, calcium ionophore A23187 and nitric oxide.缓激肽、二磷酸腺苷、钙离子载体A23187和一氧化氮对猪培养内皮细胞中环鸟苷酸生成的刺激作用。
Br J Pharmacol. 1990 Sep;101(1):152-6. doi: 10.1111/j.1476-5381.1990.tb12105.x.
2
Release of endothelium-derived relaxing factor from pig cultured aortic endothelial cells, as assessed by changes in endothelial cell cyclic GMP content, is inhibited by a phorbol ester.通过内皮细胞环磷酸鸟苷含量的变化评估,佛波酯可抑制猪主动脉内皮细胞释放内皮源性舒张因子。
Br J Pharmacol. 1990 Mar;99(3):565-71. doi: 10.1111/j.1476-5381.1990.tb12969.x.
3
Endothelium-derived relaxing factor and atriopeptin II elevate cyclic GMP levels in pig aortic endothelial cells.内皮源性舒张因子和心房肽II可提高猪主动脉内皮细胞中的环磷酸鸟苷水平。
Br J Pharmacol. 1988 Jan;93(1):229-39. doi: 10.1111/j.1476-5381.1988.tb11426.x.
4
NG-monomethyl L-arginine inhibits endothelium-derived relaxing factor-stimulated cyclic GMP accumulation in cocultures of endothelial and vascular smooth muscle cells by an action specific to the endothelial cell.NG-单甲基-L-精氨酸通过对内皮细胞具有特异性的作用,抑制内皮衍生舒张因子刺激的内皮细胞与血管平滑肌细胞共培养物中环鸟苷酸的积累。
Circ Res. 1990 Oct;67(4):979-85. doi: 10.1161/01.res.67.4.979.
5
Differential control and calcium-dependence of production of endothelium-derived relaxing factor and prostacyclin by pig aortic endothelial cells.猪主动脉内皮细胞产生内皮源性舒张因子和前列环素的差异调控及钙依赖性
Br J Pharmacol. 1989 Jul;97(3):683-90. doi: 10.1111/j.1476-5381.1989.tb12004.x.
6
Cholera toxin augments the release of endothelium-derived relaxing factor evoked by bradykinin and the calcium ionophore A23187.霍乱毒素增强缓激肽和钙离子载体A23187诱发的内皮源性舒张因子的释放。
Gen Pharmacol. 1992 Jan;23(1):27-31. doi: 10.1016/0306-3623(92)90042-i.
7
Chronic exposure of cultured endothelial cells to eicosapentaenoic acid potentiates the release of endothelium-derived relaxing factor(s).将培养的内皮细胞长期暴露于二十碳五烯酸中会增强内皮源性舒张因子的释放。
Br J Pharmacol. 1990 Jan;99(1):176-80. doi: 10.1111/j.1476-5381.1990.tb14673.x.
8
Bradykinin stimulates the production of cyclic GMP via activation of B2 kinin receptors in cultured porcine aortic endothelial cells.缓激肽通过激活培养的猪主动脉内皮细胞中的B2激肽受体来刺激环鸟苷酸的产生。
J Pharmacol Exp Ther. 1990 Feb;252(2):581-5.
9
Endothelial cyclic GMP and cyclic AMP do not regulate the release of endothelium-derived relaxing factor/nitric oxide from bovine aortic endothelial cells.内皮细胞环磷酸鸟苷和环磷酸腺苷并不调节牛主动脉内皮细胞中内皮源性舒张因子/一氧化氮的释放。
J Pharmacol Exp Ther. 1991 Feb;256(2):677-82.
10
Release of endothelin from the porcine aorta. Inhibition by endothelium-derived nitric oxide.猪主动脉中内皮素的释放。内皮源性一氧化氮的抑制作用。
J Clin Invest. 1990 Feb;85(2):587-90. doi: 10.1172/JCI114477.

引用本文的文献

1
Bradykinin B1 receptor signaling triggers complement activation on endothelial cells.缓激肽B1受体信号传导触发内皮细胞上的补体激活。
Front Immunol. 2025 Feb 7;16:1527065. doi: 10.3389/fimmu.2025.1527065. eCollection 2025.
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A novel murine in vivo model for acute hereditary angioedema attacks.一种用于急性遗传性血管性水肿发作的新型小鼠体内模型。
Sci Rep. 2021 Aug 5;11(1):15924. doi: 10.1038/s41598-021-95125-0.
3
Increased Reactive Oxygen Species Generation Contributes to the Atherogenic Activity of the B2 Bradykinin Receptor.活性氧生成增加促进B2缓激肽受体的致动脉粥样硬化活性。
Front Med (Lausanne). 2019 Feb 21;6:32. doi: 10.3389/fmed.2019.00032. eCollection 2019.
4
Identification of cytokeratin 1 as a binding protein and presentation receptor for kininogens on endothelial cells.细胞角蛋白1作为内皮细胞上激肽原的结合蛋白和呈递受体的鉴定。
Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3615-20. doi: 10.1073/pnas.95.7.3615.
5
Heparin regulates endothelin production through endothelium-derived nitric oxide in human endothelial cells.肝素通过人内皮细胞中内皮衍生的一氧化氮调节内皮素的产生。
J Clin Invest. 1993 Oct;92(4):2080-5. doi: 10.1172/JCI116805.
6
Nitric oxide pathway-mediated relaxant effect of bradykinin in the guinea-pig isolated trachea.一氧化氮途径介导的缓激肽对豚鼠离体气管的舒张作用。
Br J Pharmacol. 1994 Jan;111(1):83-8. doi: 10.1111/j.1476-5381.1994.tb14027.x.
7
Role of cyclic AMP in promoting the thromboresistance of human endothelial cells by enhancing thrombomodulin and decreasing tissue factor activities.环磷酸腺苷通过增强血栓调节蛋白和降低组织因子活性来促进人内皮细胞抗血栓形成的作用。
Br J Pharmacol. 1993 May;109(1):18-28. doi: 10.1111/j.1476-5381.1993.tb13526.x.
8
S35b, a new phenylsulfonylfuroxan compound, inhibits thrombin-induced synthesis of platelet-activating factor and prostacyclin in human endothelial cells.新型苯基磺酰基呋咱化合物S35b可抑制凝血酶诱导的人内皮细胞中血小板活化因子和前列环素的合成。
Agents Actions. 1993 Nov;40(3-4):157-65. doi: 10.1007/BF01984055.
9
Haemodynamic changes and acetylcholine-induced hypotensive responses after NG-nitro-L-arginine methyl ester in rats and cats.NG-硝基-L-精氨酸甲酯对大鼠和猫的血流动力学变化及乙酰胆碱诱导的降压反应
Br J Pharmacol. 1991 Aug;103(4):1899-904. doi: 10.1111/j.1476-5381.1991.tb12349.x.
10
The role of the L-arginine-nitric oxide pathway in relaxation of the opossum lower oesophageal sphincter.L-精氨酸-一氧化氮途径在负鼠下食管括约肌舒张中的作用。
Br J Pharmacol. 1991 Sep;104(1):113-6. doi: 10.1111/j.1476-5381.1991.tb12393.x.

本文引用的文献

1
Possible role for cyclic GMP in endothelium-dependent relaxation of rabbit aorta by acetylcholine. Comparison with nitroglycerin.环磷酸鸟苷在乙酰胆碱介导的兔主动脉内皮依赖性舒张中的可能作用。与硝酸甘油的比较。
Res Commun Chem Pathol Pharmacol. 1983 Sep;41(3):369-81.
2
Endothelium-induced relaxation by acetylcholine associated with larger rises in cyclic GMP in coronary arterial strips.乙酰胆碱引起的内皮依赖性舒张与冠状动脉条带中环鸟苷酸的更大升高有关。
J Cyclic Nucleotide Res. 1982;8(6):409-19.
3
Agonist-induced endothelium-dependent relaxation in rat thoracic aorta may be mediated through cGMP.激动剂诱导的大鼠胸主动脉内皮依赖性舒张可能通过环磷酸鸟苷(cGMP)介导。
Circ Res. 1983 Mar;52(3):352-7. doi: 10.1161/01.res.52.3.352.
4
Stimulation of cyclic AMP production by vasoactive agents in cultured bovine aortic and pulmonary artery endothelial cells.血管活性药物对培养的牛主动脉和肺动脉内皮细胞中环磷酸腺苷生成的刺激作用。
In Vitro. 1981 May;17(5):450-8. doi: 10.1007/BF02626746.
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Regulation of endothelial cell cyclic nucleotide metabolism by prostacyclin.前列环素对内皮细胞环核苷酸代谢的调节
J Clin Invest. 1981 Feb;67(2):540-6. doi: 10.1172/JCI110064.
6
Effect of adenosine on synthesis and release of cyclic AMP by cultured vascular cells from swine.腺苷对猪培养血管细胞中环磷酸腺苷合成与释放的影响。
J Cyclic Nucleotide Protein Phosphor Res. 1983;9(1):69-78.
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Endothelial cell cycle kinetics. Changes in culture and correlation with endothelial properties.内皮细胞周期动力学。培养中的变化及其与内皮特性的相关性。
Lab Invest. 1984 Dec;51(6):643-7.
8
Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor.一氧化氮的释放构成了内皮源性舒张因子的生物活性。
Nature. 1987;327(6122):524-6. doi: 10.1038/327524a0.
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Stabilization and partial characterization of endothelium-derived relaxing factor from cultured bovine aortic endothelial cells.培养的牛主动脉内皮细胞中内皮源性舒张因子的稳定化及部分特性鉴定
Biochem Biophys Res Commun. 1986 Dec 15;141(2):689-96. doi: 10.1016/s0006-291x(86)80227-3.
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L-arginine is the physiological precursor for the formation of nitric oxide in endothelium-dependent relaxation.L-精氨酸是内皮依赖性舒张中一氧化氮形成的生理前体。
Biochem Biophys Res Commun. 1988 Jun 30;153(3):1251-6. doi: 10.1016/s0006-291x(88)81362-7.

缓激肽、二磷酸腺苷、钙离子载体A23187和一氧化氮对猪培养内皮细胞中环鸟苷酸生成的刺激作用。

Stimulation of cyclic GMP production in cultured endothelial cells of the pig by bradykinin, adenosine diphosphate, calcium ionophore A23187 and nitric oxide.

作者信息

Boulanger C, Schini V B, Moncada S, Vanhoutte P M

机构信息

Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota.

出版信息

Br J Pharmacol. 1990 Sep;101(1):152-6. doi: 10.1111/j.1476-5381.1990.tb12105.x.

DOI:10.1111/j.1476-5381.1990.tb12105.x
PMID:2178013
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1917623/
Abstract
  1. The effects of bradykinin, adenosine diphosphate, calcium ionophore A23187 and nitric oxide on the production of adenosine 3':5'-cyclic monophosphate (cyclic AMP) and guanosine 3':5'-cyclic monophosphate (cyclic GMP) were investigated in cultured aortic endothelial cells of the pig. 2. Bradykinin (10(-7) M), adenosine diphosphate (3 x 10(-5) M), nitric oxide (2 x 10(-6) M) and A23187 (10(-6) M) stimulated the production of cyclic GMP. This stimulation reached a maximum within 1 min and declined rapidly with the first three agonists whereas that induced by A23187 was long-lasting. 3. These concentrations of bradykinin, A23187 and nitric oxide had no effect on cyclic AMP production. However, adenosine diphosphate (3 x 10(-5) M) slightly but significantly enhanced its production by about 1.7 fold. 4. The basal content of cyclic GMP in endothelial cells was significantly reduced by haemoglobin (10(-5) M, a scavenger of endothelium-derived relaxing factor(s] and methylene blue (10(-5) M, an inhibitor of the activation of soluble guanylate cyclase) and was significantly enhanced by superoxide dismutase (500 u ml-1, a scavenger of superoxide anions). The basal content of cyclic GMP was not affected by NG-monomethyl-L-arginine (10(-5) M, a specific inhibitor of the formation of nitric oxide from L-arginine) and was slightly but significantly increased by its D-enantiomer, NG-monomethyl-D-arginine. 5. The production of cyclic GMP stimulated by bradykinin, adenosine diphosphate, A23187 and nitric oxide was inhibited by haemoglobin (10 5M) and methylene blue (10- M) but was unaffected by superoxide dismutase (500 u ml 1)- 6. The production of cyclic GMP stimulated by bradykinin, adenosine diphosphate or A23187, but not that stimulated by nitric oxide, was significantly reduced by N0-monomethyl-L-arginine (10-M). The production of cyclic GMP evoked by nitric oxide, but not that induced by the other three agents, was enhanced significantly by N0-monomethyl-D-arginine by about 1.5 fold. 7. These data indicate that the endothelium-dependent vasodilators bradykinin, adenosine diphosphate and A23187 activate the production of cyclic GMP in endothelial cells via the synthesis of nitric oxide, which in turn stimulates the soluble guanylate cyclase.
摘要
  1. 研究了缓激肽、二磷酸腺苷、钙离子载体A23187和一氧化氮对猪主动脉内皮细胞中环磷酸腺苷(cAMP)和环磷酸鸟苷(cGMP)生成的影响。2. 缓激肽(10⁻⁷ M)、二磷酸腺苷(3×10⁻⁵ M)、一氧化氮(2×10⁻⁶ M)和A23187(10⁻⁶ M)刺激了cGMP的生成。这种刺激在1分钟内达到最大值,前三种激动剂作用下其迅速下降,而A23187诱导的则是持久的。3. 这些浓度的缓激肽、A23187和一氧化氮对cAMP的生成没有影响。然而,二磷酸腺苷(3×10⁻⁵ M)轻微但显著地将其生成提高了约1.7倍。4. 血红蛋白(10⁻⁵ M,一种内皮源性舒张因子清除剂)和亚甲蓝(10⁻⁵ M,一种可溶性鸟苷酸环化酶激活抑制剂)显著降低了内皮细胞中cGMP的基础含量,而超氧化物歧化酶(500 U/ml,一种超氧阴离子清除剂)则显著提高了其基础含量。cGMP的基础含量不受N⁰-甲基-L-精氨酸(10⁻⁵ M,一种从L-精氨酸形成一氧化氮的特异性抑制剂)的影响,而其D-对映体N⁰-甲基-D-精氨酸则使其轻微但显著增加。5. 缓激肽、二磷酸腺苷、A23187和一氧化氮刺激的cGMP生成受到血红蛋白(10⁻⁵ M)和亚甲蓝(10⁻⁵ M)的抑制,但不受超氧化物歧化酶(500 U/ml)的影响。6. 缓激肽、二磷酸腺苷或A23187刺激的cGMP生成,但一氧化氮刺激的cGMP生成不受影响,被N⁰-甲基-L-精氨酸(10⁻⁵ M)显著降低。一氧化氮诱发的cGMP生成,但不是其他三种试剂诱导的cGMP生成,被N⁰-甲基-D-精氨酸显著提高了约1.5倍。7. 这些数据表明,内皮依赖性血管舒张剂缓激肽、二磷酸腺苷和A23187通过一氧化氮的合成激活内皮细胞中cGMP的生成,进而刺激可溶性鸟苷酸环化酶。