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本研究采用全细胞膜片钳技术观察了SNC162 (一种选择性δ阿片受体激动剂)对大鼠心室肌细胞L型钙电流(L-type Ca2+current, ICa-L)和瞬时外向钾电流(transient outward K+ current, Ito)的影响。结果显示,SNC162 明显抑制大鼠心室肌细胞 ICa-L 和Ito,对 ICa-L 和 Ito 的最大抑制率分别为(46.13±4.12)% 和(36.53±10.57)%。1×10-4 mol/L SNC162 使 ICa-L 的平均电流密度从(8.98±0.40) pA/pF下降到(4.84±0.44) pA/pF (P<0.01, n=5),Ito 的平均电流密度从(18.69±2.42) pA/pF降低到(11.73±1.67) pA/pF (P<0.01,n=5)。单独应用 naltrindole (一种选择性δ阿片受体拮抗剂)对大鼠心室肌细胞 ICa-L 和 Ito 无显著作用,但预先应用 naltrindole 可以消除SNC162 对ICa-L和Ito 的抑制作用。结果表明,通过δ阿片受体,SNC162 (1×10-6~1×10-4 mol/L)浓度依赖性地抑制大鼠心室肌细胞ICa-L 和 Ito,这可能是激动δ阿片受体产生抗心律失常效应的重要机制。
In this study, whole-cell patch-clamp technique was used to observe the effects of SNC162, a selective δ-opioid receptor agonist, on L-type Ca2 + current (ICa-L) and transient outward potassium currents (transient outward K + current, Ito) influence. The results showed that SNC162 significantly inhibited ICa-L and Ito in rat ventricular myocytes, and the maximum inhibitory rates of ICa-L and Ito were (46.13 ± 4.12)% and (36.53 ± 10.57)%, respectively. The average current density of ICa-L decreased from (8.98 ± 0.40) pA / pF to (4.84 ± 0.44) pA / pF (P <0.01, n = 5) in 1 × 10-4 mol / L SNC162. The density decreased from (18.69 ± 2.42) pA / pF to (11.73 ± 1.67) pA / pF (P <0.01, n = 5). Single administration of naltrindole, a selective delta opioid receptor antagonist, had no significant effect on ICa-L and Ito in rat ventricular myocytes, but pretreatment with naltrindole abolished the inhibitory effect of SNC162 on ICa-L and Ito. The results showed that SNC162 (1 × 10-6 ~ 1 × 10-4 mol / L) inhibited the ICa-L and Ito of rat ventricular myocytes in a concentration-dependent manner through δ opioid receptor, which may be an agonist of δ opioid receptor An important mechanism to produce anti-arrhythmic effects.