N-Methyl-2-pyridone-5-carboxamide 是 1-methylnicotinamide 代谢物，具有低环氧合酶依赖性血管舒张活性。,Journal of Physiology and Biochemistry

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N-Methyl-2-pyridone-5-carboxamide 是 1-methylnicotinamide 代谢物，具有低环氧合酶依赖性血管舒张活性。
Journal of Physiology and Biochemistry ( IF 3.7 ) Pub Date : 2012-01-13 , DOI: 10.1007/s13105-012-0144-4
Tomasz Przygodzki ₁ , Bartlomiej Grobelski , Piotr Kazmierczak , Cezary Watala

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1-甲基烟酰胺 (MNA) 是烟酰胺的主要代谢物，最近被证实可导致 PGI ₂血浆水平以未知机制全身性升高。我们目前的研究旨在验证 PGI ₂（一种血管舒张类前列腺素）的产生是否可以在体外条件下复制，以响应 MNA、其代谢物N-甲基-2-吡啶酮-5-甲酰胺（Met2PY）和烟酰胺. 由于前列环素是一种血管舒张类前列腺素，我们还在体外冠状血管床灌注模型中进行了功能测试，以评估这些化合物的血管活性。我们没有观察到测试药物对 PGI ₂或 PGE _{2 的}任何显着影响在我们的体外模型中分泌。浓度为 10 和 100 μmol/l 以及 100 μmol/l Met2PY 的烟酰胺略微但显着增加了大鼠心脏中的冠状动脉血流。然而，与参考化合物缓激肽 (100 nmol/l) 引起的增加相比，这些增加仍然很低。在 50 μmol/l 吲哚美辛存在下用 Met2PY 灌注大鼠心脏导致冠状动脉血流减少，这证明该作用是环加氧酶依赖性的。我们得出的结论是，MNA 代谢物应该在前列环素原活性方面得到更仔细的处理，并且 MNA 诱导 PGI ₂产生的系统机制需要进一步澄清。

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N-Methyl-2-pyridone-5-carboxamide is 1-methylnicotinamide metabolite of low cyclooxygenase-dependent vasodilating activity.

1-Methylnicotinamide (MNA) is a primary metabolite of nicotinamide recently proven to cause systemic increase in PGI₂ plasma levels in an unknown mechanism. Our present study was aimed at verifying whether the increased production of PGI₂, a vasodilating prostanoid, in response to MNA, its metabolite N-methyl-2-pyridone-5-carboxamide (Met2PY), and nicotinamide may be reproduced under in vitro conditions. Since prostacyclin is a vasodilating prostanoid, we also performed the functional tests in the ex vivo model of coronary vascular bed perfusion to evaluate the vasoactive properties of those compounds. We did not observe any significant effect of the tested drugs on either PGI₂ or PGE₂ secretion in our in vitro model. Nicotinamide at the concentrations of 10 and 100 μmol/l and 100 μmol/l Met2PY slightly but significantly increased coronary flow in rat heart. These increases, however, remained very low when compared to that induced by the reference compound, bradykinin (100 nmol/l). Perfusion of rat hearts with Met2PY in the presence of 50 μmol/l indomethacin resulted in decreased coronary flow, which proves that the effect is cyclooxygenase dependent. We conclude that MNA metabolites should be more carefully addressed in reference to pro-prostacyclin activity and that systemic mechanism of MNA-induced PGI₂ production needs further clarification.

更新日期：2012-01-13

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