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首页> 外文期刊>Life sciences >PHARMACOLOGICAL NATURES OF CAFFEINE-INDUCED ENDOTHELIUM-DEPENDENT AND -INDEPENDENT CONTRACTION IN CANINE MESENTERIC ARTERY
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PHARMACOLOGICAL NATURES OF CAFFEINE-INDUCED ENDOTHELIUM-DEPENDENT AND -INDEPENDENT CONTRACTION IN CANINE MESENTERIC ARTERY

机译：咖啡因诱导的犬中肠动脉内皮依赖性和非依赖性收缩的药理学性质

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摘要

The present experiments were carried out to elucidate whether pharmacological nature of caffeine (1 mM)-induced endothelium-dependent contraction (EDC) is different from that of caffeine (10 mM)-induced endothelium-independent contraction (EIC) in canine mesenteric artery. Caffeine (1 mM)-induced EDC was abolished when arterial strips were incubated in Ca++-free medium for 20 min, but EIC was not abolished. EGTA and EDTA (0.5 and 1 mM) attenuated the EDC, and at the concentration of 2.5 mM completely abolished the EDC. Nifedipine (10(-6) and 3 x 10(-6) M), diltiazem (10(-6) M) and verapamil (10(-6) M) did not affect the caffeine (1 mM)-induced EDC. Lemakalim (10(-8), 3 x 10(-8) and 10(-7) M) attenuated the caffeine (1 mM)-induced EDC in a concentration-dependent manner. Lemakalim (10(-7) M) nearly abolished the EDC. The inhibitory effect of lemakalim (10(-7) M) on the EDC was antagonized in the presence of glibenclamide (3 x 10(-6) M). In contrast, caffeine (10 mM)-induced EIC was resistant to lemakalim at higher concentration (3 x 10(-7) M). Forskolin (10(-7), 3 x 10(-7) and 10(-6) M) significantly attenuated both the caffeine (1 mM)-induced EDC and caffeine (10 mM)-induced EIC. The inhibitory effect of forskolin on the EDC was augmented in the presence of rolipram (10(-6) M). Nitroglycerin (10(-5) M) attenuated significantly caffeine-induced both EDC and EIC. The inhibitory effect of nitroglycerin on the EDC was augmented in the presence of zaprinast (10(-5) M). The present experiments demonstrate that zcaffeine-induced EDC is due to nifedipine-resistant and lemakalim-sensitive Ca++ mobilization and the EIC is due to both nifedipine- and lemakalim-resistant Ca++ mobilization in canine mesenteric artery. [References: 21]
机译：进行本实验以阐明在犬肠系膜动脉中咖啡因（1 mM）诱导的内皮依赖性收缩（EDC）与咖啡因（10 mM）诱导的内皮依赖性收缩（EIC）的药理性质是否不同。当在不含Ca ++的培养基中孵育动脉条20分钟时，咖啡因（1 mM）诱导的EDC被消除，但EIC未被消除。 EGTA和EDTA（0.5和1 mM）使EDC衰减，在2.5 mM的浓度下，EDC完全消失。硝苯地平（10（-6）和3 x 10（-6）M），地尔硫卓（10（-6）M）和维拉帕米（10（-6）M）不会影响咖啡因（1 mM）诱导的EDC。 Lemakalim（10（-8），3 x 10（-8）和10（-7）M）以浓度依赖的方式减弱了咖啡因（1 mM）诱导的EDC。 Lemakalim（10（-7）M）几乎废除了EDC。在格列本脲（3 x 10（-6）M）存在的情况下，lemakalim（10（-7）M）对EDC的抑制作用被拮抗。相反，咖啡因（10 mM）诱导的EIC在较高浓度（3 x 10（-7）M）下对lemakalim具有抗性。 Forskolin（10（-7），3 x 10（-7）和10（-6）M）显着减弱了咖啡因（1 mM）诱导的EDC和咖啡因（10 mM）诱导的EIC。在存在咯利普兰（10（-6）M）的情况下，毛喉素对EDC的抑制作用增强。硝酸甘油（10（-5）M）大大减弱了咖啡因诱导的EDC和EIC。在存在扎必利斯特（10（-5）M）的情况下，硝酸甘油对EDC的抑制作用增强。本实验表明，咖啡因诱导的EDC是由于犬肠系膜动脉中的硝苯地平抗性和来马卡林敏感的Ca ++动员引起的，而EIC是由于硝苯地平和耐lemakalim的Ca ++动员引起的。 [参考：21]

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