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氯化铵对大鼠主动脉血管收缩增强作用的机制

Mechanism of the potentiating effect of NH4Cl on vasoconstriction in rat aorta.

作者信息

Tanaka H, Wakabayashi I, Sakamoto K, Kakishita E

机构信息

Second Department of Internal Medicine, Hyogo College of Medicine, Japan.

出版信息

Gen Pharmacol. 1996 Apr;27(3):535-8. doi: 10.1016/0306-3623(95)00104-2.

Abstract
  1. In medium containing 10 or 20 mM KCl, NH4Cl (10 mM) addition significantly diminished tetraphenylphosphonium bromide (TPP+) uptake in A7r5 vascular smooth muscle cells. 2. Addition of 10 mM NH4Cl significantly potentiated the 45Ca2+ uptake of A7r5 cells in medium containing 20 mM KCl; this increased uptake could be reduced to the basal level by pretreatment with 0.1 microM verapamil. 3. In rat aortic strips, KCl at 10 mM induced a slight contraction, that was greatly potentiated by the simultaneous addition of 10 mM NH4Cl. In this case, also, pretreatment with verapamil (1 microM) completely abolished the NH4Cl-potentiating effect. 4. The results suggest that ammonium ion amplifies the K(+)-induced contraction of rat aorta by facilitating transmembraneous Ca2+ influx through the voltage-dependent calcium channel, which may be due to potentiation of KCl-induced depolarization of the plasma membrane.
摘要
  1. 在含有10或20 mM氯化钾的培养基中,添加10 mM氯化铵会显著减少A7r5血管平滑肌细胞对溴化四苯基鏻(TPP+)的摄取。2. 在含有20 mM氯化钾的培养基中,添加10 mM氯化铵可显著增强A7r5细胞对45Ca2+的摄取;这种增加的摄取可通过用0.1 microM维拉帕米预处理降低至基础水平。3. 在大鼠主动脉条中,10 mM氯化钾引起轻微收缩,同时添加10 mM氯化铵可使其显著增强。同样在这种情况下,用1 microM维拉帕米预处理可完全消除氯化铵的增强作用。4. 结果表明,铵离子通过促进跨膜Ca2+经电压依赖性钙通道内流来放大钾离子诱导的大鼠主动脉收缩,这可能是由于增强了氯化钾诱导的质膜去极化。

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