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首页> 外文期刊>Life sciences >Endothelium-dependent and -independent vasorelaxation by a theophylline derivative MCPT: Roles of cyclic nucleotides, potassium channel opening and phosphodiesterase inhibition.
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Endothelium-dependent and -independent vasorelaxation by a theophylline derivative MCPT: Roles of cyclic nucleotides, potassium channel opening and phosphodiesterase inhibition.

机译：茶碱衍生物MCPT的内皮依赖性和非依赖性血管舒张：环状核苷酸，钾通道开放和磷酸二酯酶抑制的作用。

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The vasorelaxation activities of MCPT, a newly synthesized xanthine derivative, were investigated in this study. In phenylephrine (PE)-precontracted rat aortic rings with intact endothelium, MCPT caused a concentration-dependent relaxation, which was inhibited by endothelium removed. This relaxation was also reduced by the presence of nitric oxide synthase inhibitor L(omega)-nitro-L-arginine methylester (L-NAME, 100 muM), soluble guanylyl cyclase (sGC) inhibitors methylene blue (10 muM), 1 H-[1,2,4] oxidazolol [4,3-a] quinoxalin-1-one (ODQ, 1 muM), adenylyl cyclase (AC) blocker SQ 22536 (100 muM), ATP-sensitive K(+) channel blocker (K(ATP)) glibenclamide (1 muM), a Ca(2+) activated K(+) channels blocker tetraethylammonium (TEA, 10 mM) and a voltage-dependent potassium channels blocker 4-aminopyridine (4-AP, 100 muM). The vasorelaxant effects of MCPT together with IBMX (0.5 muM) had an additive action. In PE-preconstricted endothelium-denuded aortic rings, the vasorelaxant effects of MCPT were attenuated by pretreatments with glibenclamide (1 muM), SQ 22536 (100 muM) or ODQ (1 muM), respectively. MCPT enhanced cAMP-dependent vasodilator isoprenaline- and NO donor/cGMP-dependent vasodilator sodium nitroprusside-induced relaxation activities in endothelium-denuded aortic rings. In A-10 cell and washed human platelets, MCPT induced a concentration-dependent increase in intracellular cyclic GMP and cyclic AMP levels. In phosphodiesterase assay, MCPT displayed inhibition effects on PDE 3, PDE 4 and PDE 5. The inhibition % were 52 +/- 3.9, 32 +/- 2.6 and 8 +/- 1.1 respectively. The Western blot analysis on HUVEC indicated that MCPT increased the expression of eNOS. It is concluded that the vasorelaxation by MCPT may be mediated by the inhibition of phosphodiesterase, stimulation of NO/sGC/ cGMP and AC/cAMP pathways, and the opening of K(+) channels.
机译：本研究研究了新合成的黄嘌呤衍生物MCPT的血管舒张活性。在带有完整内皮的去氧肾上腺素（PE）收缩的大鼠主动脉环中，MCPT引起了浓度依赖性的舒张，该舒张受到内皮去除的抑制。一氧化氮合酶抑制剂L（ω）-硝基-L-精氨酸甲酯（L-NAME，100μM），可溶性鸟苷基环化酶（sGC）抑制剂亚甲基蓝（10μM），1 H- [1,2,4]氧化唑[4,3-a]喹喔啉-1-酮（ODQ，1μM），腺苷酸环化酶（AC）阻滞剂SQ 22536（100μM），ATP敏感的K（+）通道阻滞剂（ K（ATP））格列本脲（1μM），Ca（2+）激活的K（+）通道阻滞剂四乙铵（TEA，10 mM）和电压依赖性钾通道阻滞剂4-氨基吡啶（4-AP，100μM） 。 MCPT与IBMX（0.5μM）的血管舒张作用具有累加作用。在PE预收缩的内皮剥脱的主动脉环中，分别用glibenclamide（1μM），SQ 22536（100μM）或ODQ（1μM）预处理减弱了MCPT的血管舒张作用。 MCPT增强了cAMP依赖性血管扩张剂异戊二烯和NO供体/ cGMP依赖性血管扩张剂硝普钠诱导的内皮剥除主动脉环的舒张活性。在A-10细胞和洗涤过的人血小板中，MCPT诱导了细胞内环状GMP和环状AMP水平的浓度依赖性增加。在磷酸二酯酶测定中，MCPT显示出对PDE 3，PDE 4和PDE 5的抑制作用。抑制％分别为52 +/- 3.9、32 +/- 2.6和8 +/- 1.1。 HUVEC的蛋白质印迹分析表明MCPT增加了eNOS的表达。结论是，MCPT的血管舒张作用可能是通过抑制磷酸二酯酶，刺激NO / sGC / cGMP和AC / cAMP途径以及打开K（+）通道而介导的。

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