首页> 外文期刊>Endothelium: Journal of endothelial cell research >Insulin preincubation effects on rat vessel contractile responses: role of the sarcoplasmic reticulum.
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Insulin preincubation effects on rat vessel contractile responses: role of the sarcoplasmic reticulum.

机译:胰岛素预培养对大鼠血管收缩反应的影响:肌浆网的作用。

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摘要

In the present work, we studied the possible mechanisms involved in the insulin-induced acceleration of ET1 contractions. We observed a shortening of the half-life needed to achieve maximal developed force (t(1/2)) at 10(-7) M ET1 in rat aortic rings preincubated for 120 min with 3 nM insulin (control 380 +/- 15 s vs. 319 +/- 8 s with insulin, n = 28, p < 0.05). A tyrosine kinase linked receptor was involved in this effect because it was abolished by 30 microM genistein. Endothelium denudation and 10 microM indomethacin treatment did not effect this insulin effect, suggesting its independence of endothelial-derived factors. The effect was still present when the only source of Ca2+ was intracellular (t(1/2) values in the absence of external Ca2+: control 467 +/- 68 s vs. 213 +/- 28 s with insulin, n = 16, p < 0.05), but was blunted if the sarcoplasmic reticulum (SR) Ca2+ source was suppressed by exposure to 10 microM thapsigargin or 10 microM ryanodine. Preincubation with insulin did not potentiate either SR 45Ca2+ uptake or contractions evoked by caffeine-sensitive SR Ca2+ release. Since 30 microM cheleritrine abolished insulin-induced acceleration of ET1 contractions, we propose that the hormone might enhance a signal pathway related to PKC in order to produce a faster Ca2+ release from the SR.
机译:在目前的工作中,我们研究了胰岛素诱导的ET1收缩加速的可能机制。我们观察到在大鼠主动脉环中与3 nM胰岛素预孵育120分钟时,在10(-7)M ET1处达到最大显影力(t(1/2))所需的半衰期缩短(对照380 +/- 15 s与319 +/- 8 s胰岛素相比,n = 28,p <0.05)。酪氨酸激酶连接的受体参与了这种作用,因为它被30 microM染料木黄酮废除了。内皮剥脱术和10 microM消炎痛治疗并不影响这种胰岛素作用,提示其与内皮衍生因子无关。当唯一的Ca2 +来源是细胞内(t(1/2)值而不存在外部Ca2 +时)仍然存在该效果:对照467 +/- 68 s与胰岛素的213 +/- 28 s,n = 16 p <0.05),但是如果肌浆网(SR)Ca2 +来源通过暴露于10 microM毒胡萝卜素或10 microM ryanodine而受到抑制,则会变钝。胰岛素预孵育不能增强SR 45Ca2 +的摄取或咖啡因敏感性SR Ca2 +释放引起的收缩。由于30 microM的苦参碱消除了胰岛素诱导的ET1收缩加速,因此我们建议该激素可能增强与PKC相关的信号通路,以便从SR释放更快的Ca2 +。

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