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本文引用的文献

1
The regulation of aortic endothelial cells by purines and pyrimidines involves co-existing P2y-purinoceptors and nucleotide receptors linked to phospholipase C.嘌呤和嘧啶对主动脉内皮细胞的调节涉及与磷脂酶C相关的共存P2y嘌呤受体和核苷酸受体。
Br J Pharmacol. 1993 Mar;108(3):689-93. doi: 10.1111/j.1476-5381.1993.tb12862.x.
2
Heterogeneity of ATP receptors in aortic endothelial cells. Involvement of P2y and P2u receptors in inositol phosphate response.主动脉内皮细胞中ATP受体的异质性。P2y和P2u受体参与肌醇磷酸反应。
Circ Res. 1993 Mar;72(3):504-10. doi: 10.1161/01.res.72.3.504.
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A2-purinoceptor-mediated relaxation in the guinea-pig coronary vasculature: a role for nitric oxide.A2嘌呤受体介导的豚鼠冠状血管舒张：一氧化氮的作用
Br J Pharmacol. 1993 Jun;109(2):424-9. doi: 10.1111/j.1476-5381.1993.tb13586.x.
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Stimulation of vascular prostacyclin synthesis by extracellular ADP and ATP.细胞外二磷酸腺苷（ADP）和三磷酸腺苷（ATP）对血管前列环素合成的刺激作用。
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Stimulation of prostaglandin production through purinoceptors on cultured porcine endothelial cells.通过培养的猪内皮细胞上的嘌呤受体刺激前列腺素生成。
Biochem J. 1983 Jul 15;214(1):273-6. doi: 10.1042/bj2140273.
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The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine.内皮细胞在乙酰胆碱介导的动脉平滑肌舒张中所起的不可或缺的作用。
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Purinoceptor mediated stimulation of prostacyclin release in the porcine pulmonary vasculature.嘌呤受体介导的猪肺血管中前列环素释放的刺激作用。
Br J Pharmacol. 1984 Oct;83(2):457-62. doi: 10.1111/j.1476-5381.1984.tb16507.x.
8
Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs.抑制前列腺素合成作为阿司匹林类药物的作用机制。
Nat New Biol. 1971 Jun 23;231(25):232-5. doi: 10.1038/newbio231232a0.
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Adenine-, guanine- and uridine-5'-phosphonucleotides in blood platelets and storage organelles of various species.
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10
Stimulation of prostaglandin biosynthesis by adenine nucleotides. Profile of prostaglandin release by perfused organs.腺嘌呤核苷酸对前列腺素生物合成的刺激作用。灌注器官释放前列腺素的概况。
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嘧啶对豚鼠冠状血管系统的影响。

Effects of pyrimidines on the guinea-pig coronary vasculature.

作者信息

Vials A J, Burnstock G

机构信息

Department of Anatomy and Developmental Biology, University College London.

出版信息

Br J Pharmacol. 1993 Nov;110(3):1091-7. doi: 10.1111/j.1476-5381.1993.tb13926.x.

DOI:10.1111/j.1476-5381.1993.tb13926.x
PMID:8298797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2175825/
Abstract
  1. The effects of the pyrimidines, uridine 5'-triphosphate (UTP), thymidine 5'-triphosphate (TTP) and cytidine 5'-triphosphate (CTP), were examined in the guinea-pig coronary bed, by use of a Langendorff technique. Comparisons were made with the actions of the purines adenosine 5'-triphosphate (ATP), inosine 5'-triphosphate (ITP) and guanosine 5'-triphosphate (GTP). The effect of, the nitric oxide synthase inhibitor, L-NG-nitroarginine methyl ester (L-NAME) and, the prostaglandin synthesis inhibitor, indomethacin on the vasodilator response to these purines and pyrimidines was examined. The effects of these inhibitors were assessed on their ability to inhibit both the amplitude and the area of the vasodilator response. 2. The relative order of potency of the purines and pyrimidines studied was ATP > UTP > ITP >> GTP, TTP, CTP. 3. The maximum amplitude and area of the vasodilator response to the pyrimidines, UTP (5 x 10(-10)-5 x 10(-7) mol), TTP (5 x 10(-8)-5 x 10(-7) mol) and CTP (5 x 10(-7) mol), and purines, ITP (5 x 10(-9)-5 x 10(-7) mol) and GTP (5 x 10(-8)-5 x 10(-7) mol), were significantly reduced by L-NAME (3 x 10(-5) and 10(-4) M). 4. The inhibition of the response to ATP (5 x 10-8 mol), UTP (5 x 10-8 mol), ITP (5 x 10-8 mol), TTP(5 x 10-7 mol), CTP (5 x 10- mol) and GTP (5 x 10- mol) by L-NAME (3 x 10-5 M) was significantly reversed by L-arginine (1.5 x 10-3 M).5. L-NAME (3 x 10-5 and 10-4 M) only inhibited the amplitude of the vasodilator response to a low dose of ATP (5 x 10-mol), although the area of vasodilator response to ATP(5 x 10-11-5 x 10-7 mol) was significantly reduced by L-NAME (3 x 10-5 and 10-4 M).6. The maximum amplitude of the vasodilator response to ATP (5 x 10-10-5 x 10-7 mol) was significantly reduced by indomethacin (10-6 M), although the area of the vasodilator response to ATP was only significantly reduced at one intermediate dose (5 x 10-9 mol). Indomethacin (10-6 M) did not affect the maximum amplitude or area of the vasodilator responses to UTP (5 x 10-11-5 x 10-7 mol),ITP (5 x 10-10-5 x 10-7 mol), CTP (5 x 10-7 mol), TTP (5 x 10-8-5 x 10-7 mol) and GTP(5 x 10-8-5 x 10-7 mol).7. It is concluded that in the guinea-pig coronary vasculature, the vasodilatation evoked by the pyrimidines, UTP, TTP and CTP, was mediated in large part via nitric oxide, as were the vasodilatations evoked by the purines ITP and GTP. The vasodilatations evoked by ATP, however, appear to involve prostanoids in addition to the release of nitric oxide.
摘要
  1. 采用Langendorff技术，在豚鼠冠状动脉床中研究了嘧啶类物质尿苷5'-三磷酸（UTP）、胸苷5'-三磷酸（TTP）和胞苷5'-三磷酸（CTP）的作用。并与嘌呤类物质腺苷5'-三磷酸（ATP）、肌苷5'-三磷酸（ITP）和鸟苷5'-三磷酸（GTP）的作用进行了比较。研究了一氧化氮合酶抑制剂L-NG-硝基精氨酸甲酯（L-NAME）和前列腺素合成抑制剂吲哚美辛对这些嘌呤和嘧啶类物质血管舒张反应的影响。通过评估这些抑制剂抑制血管舒张反应的幅度和面积的能力来评价其作用效果。2. 所研究的嘌呤和嘧啶类物质的效力相对顺序为ATP > UTP > ITP >> GTP、TTP、CTP。3. L-NAME（3×10⁻⁵和10⁻⁴ M）可显著降低嘧啶类物质UTP（5×10⁻¹⁰ - 5×10⁻⁷ mol）(、)TTP（5×10⁻⁸ - 5×10⁻⁷ mol）和CTP（5×10⁻⁷ mol）以及嘌呤类物质ITP（5×10⁻⁹ - 5×10⁻⁷ mol）和GTP（5×10⁻⁸ - 5×10⁻⁷ mol）引起的血管舒张反应的最大幅度和面积。4. L-精氨酸（1.5×10⁻³ M）可显著逆转L-NAME（3×10⁻⁵ M）对ATP（5×10⁻⁸ mol）(、)UTP（5×10⁻⁸ mol）(、)ITP（5×10⁻⁸ mol）(、)TTP（5×10⁻⁷ mol）(、)CTP（5×10⁻⁷ mol）和GTP（5×10⁻⁷ mol）反应的抑制作用。5. L-NAME（3×10⁻⁵和10⁻⁴ M）仅抑制低剂量ATP（5×10⁻¹¹ mol）引起的血管舒张反应的幅度，尽管L-NAME（3×10⁻⁵和10⁻⁴ M）可显著降低ATP（5×10⁻¹¹ - 5×10⁻⁷ mol）引起的血管舒张反应面积。6. 吲哚美辛（10⁻⁶ M）可显著降低ATP（5×10⁻¹⁰ - 5×10⁻⁷ mol）引起的血管舒张反应的最大幅度，尽管仅在一个中间剂量（5×10⁻⁹ mol）下ATP引起的血管舒张反应面积显著降低。吲哚美辛（10⁻⁶ M）不影响UTP（5×10⁻¹¹ - 5×10⁻⁷ mol）(、)ITP（5×10⁻¹⁰ - 5×10⁻⁷ mol）(、)CTP（5×10⁻⁷ mol）(、)TTP（5×10⁻⁸ - 5×`10⁻⁷ mol）和GTP（5×10⁻⁸ - 5×10⁻⁷ mol）引起的血管舒张反应的最大幅度或面积。7. 得出结论：在豚鼠冠状血管系统中，嘧啶类物质UTP、TTP和CTP引起的血管舒张在很大程度上是通过一氧化氮介导的，嘌呤类物质ITP和GTP引起的血管舒张也是如此。然而，ATP引起的血管舒张除了一氧化氮的释放外，似乎还涉及前列腺素。