首页> 外文期刊>Japanese Journal of Pharmacology >Mechanisms of the Enhanced Contractile Response to a Low Concentration of Phorbol 12, 13-Dibutyrate in Thoracic Aorta Isolated from Rats with Dietary Magnesium Deficiency
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Mechanisms of the Enhanced Contractile Response to a Low Concentration of Phorbol 12, 13-Dibutyrate in Thoracic Aorta Isolated from Rats with Dietary Magnesium Deficiency

机译:饮食性镁缺乏症大鼠胸主动脉中低浓度Phorbol 12、13-二丁酸增强收缩反应的机制

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References(29) Cited-By(1) The mechanisms underlying the enhanced contractile response to phorbol 12, 13-dibutyrate (PDBu) were examined in de-endothelialized thoracic aortas isolated from rats with dietary magnesium (Mg) deficiency. PDBu (1.0 nM)-induced contractions were significantly larger in Mg-deficient rats than in the controls. The contraction was completely inhibited by nifedipine, removal of external Ca2+ or by l-(5-isoquinolinesulfonyl)-2-methylpiperazine (H7). PDBu (1.0 nM) and phorbol 12-myristate 13-acetate (1.0μM) significantly decreased the KD value and increased the Bmax for the binding of [3H]PN200-110 to the aortas. The degree of the decrease in the KD value was significantly greater in Mg-deficient rats than in the controls. The PDBu-induced decrease in the KD value was abolished by H7. These results suggest that activation of protein kinase C by phorbol esters may participate in the activation of L-type Ca2+ channels, which increases both the affinity of [3H]PN200-110 binding and the magnitude of the external Ca2+-dependent contraction. Dietary Mg-deficiency may enhance these processes.
机译:参考文献(29)被引用(1)在从饮食缺乏镁(Mg)的大鼠中分离的去内皮化胸主动脉中研究了对佛波醇12、13-二丁酸(PDBu)增强收缩反应的潜在机制。缺镁大鼠中PDBu(1.0 nM)引起的收缩明显大于对照组。硝苯地平,外部Ca2 +的去除或1-(5-异喹啉磺酰基)-2-甲基哌嗪(H7)完全抑制了收缩。 PDBu(1.0 nM)和佛波醇12-肉豆蔻酸酯13-乙酸酯(1.0μM)显着降低了KD值,并增加了[3H] PN200-110与主动脉结合的Bmax。缺镁大鼠的KD值降低程度明显高于对照组。 H7消除了PDBu引起的KD值下降。这些结果表明佛波酯对蛋白激酶C的激活可能参与L型Ca2 +通道的激活,这既增加了[3H] PN200-110结合的亲和力,又增加了外部Ca2 +依赖性收缩的幅度。饮食中镁缺乏可能会增强这些过程。

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