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Insulin effects on the sympathetic contraction of rabbit ear arteries.

机译:胰岛素对兔耳动脉交感收缩的影响。

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Electrical field stimulation (4 Hz, 0.2 ms, 70 V supramaximal voltage, 10 s duration) produced contraction of perfused rabbit central ear arteries, and this contraction was reduced by incubation with insulin (0.6--200 mU/ml). This inhibitory effect of insulin was not significantly modified by removing the endothelium, or by treatment with N(W)-nitro-L-arginine (L-NA, 10(-4) M), meclofenamate (10(-5) M), ouabain (10(-6) M), or cocaine (10(-5) M). Insulin (200 mU/ml) did not modify the vascular contraction due to exogenous norepinephrine (10(-8)--10(-4) M) nor the relaxation due to acetylcholine (10(-8)--10(-4) M). This suggests that insulin may reduce vascular contraction by sympathetic stimulation, and this effect is not dependent on endothelial nitric oxide, prostanoids, or Na(+)--K(+) pump activation.
机译:电场刺激(4 Hz,0.2 ms,最高电压70 V,持续10 s的持续时间)产生了灌注的兔中央耳动脉的收缩,并且通过与胰岛素孵育(0.6--200 mU / ml)减少了这种收缩。通过去除内皮或用N(W)-硝基-L-精氨酸(L-NA,10(-4)M),甲氯芬那酸盐(10(-5)M)处理,胰岛素的这种抑制作用没有明显改变。 ,哇巴因(10(-6)M)或可卡因(10(-5)M)。胰岛素(200 mU / ml)不会改变由于外源去甲肾上腺素(10(-8)-10(-4)M)引起的血管收缩,也不会因乙酰胆碱(10(-8)-10(-4) )M)。这表明胰岛素可以通过交感神经刺激来减少血管收缩,并且这种作用不依赖于内皮一氧化氮,前列腺素或Na(+)-K(+)泵的激活。

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