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目的研究二甲基氨氯吡咪(DMA)对高钾预收缩大鼠主动脉血管环的效应及其可能的机制。方法采用离体血管环实验方法,记录KCl(30 mmol/L)预收缩的离体大鼠主动脉环张力变化,观察DMA对大鼠主动脉血管环的作用及不同工具药的影响。结果二甲基氨氯吡咪(1×10-6mol/L～3×10-5mol/L)对基础状态的大鼠主动脉血管环无作用,而对KCl(30 mmol/L)引起的大鼠主动脉血管环的张力变化有浓度依赖性的收缩作用,最大收缩率为(30.49±4.11)%,EC50为5.38 mol/L±1.68 mol/L。DMA可使CaCl2量效曲线非平行左上移,在KCl预收缩基础上,钠钙交换体的阻滞剂KB-R7943、钙通道阻滞剂尼卡地平、Na+-K+-ATP酶阻滞剂洋地黄均可抑制二甲基氨氯吡咪对血管的收缩作用。结论二甲基氨氯吡咪对KCl引起的血管收缩有浓度依赖性的进一步收缩作用,此作用可能与DMA促进细胞外钙内流有关,与血管平滑肌上的钠钙交换体,L-型钙通道以及Na+-K+-ATP酶有关。
Objective To investigate the effect of DMA on the aortic vascular rings in rats pre-contracted by high potassium and its possible mechanism. Methods The in vitro vascular ring test was used to record the changes of aortic ring tension of precontracted isolated KCl rats (30 mmol / L). The effects of DMA on the aortic rings and the effects of different tools were observed. Results Dimethyl amiloride (1 × 10-6mol / L ~ 3 × 10-5mol / L) had no effect on the basic aortic vascular rings in rats, but the effects of KCl (30 mmol / L) The changes of the tension of rat aorta ring in a concentration-dependent manner showed that the maximal contraction rate was (30.49 ± 4.11)% and the EC50 was 5.38 mol / L ± 1.68 mol / L. DMA can CaCl2 dose-effect curve non-parallel shift to the left, based on KCl precontraction, sodium-calcium exchanger blockers KB-R7943, calcium channel blocker nicardipine, Na + -K + -ATPase blocker foreign Rehmannia can inhibit dimethylamlril on vascular contraction. CONCLUSION: Dimethyl amiloride has a further dose-dependent contraction effect on vasoconstriction induced by KCl. This effect may be related to the effect of DMA on extracellular calcium influx, which is related to the increase of sodium-calcium exchanger, L-type calcium Channel and Na + -K + -ATP enzyme.