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目的:探究他克莫司对大鼠胸主动脉的舒张作用及其机制。方法:采用多道生理记录仪测定大鼠胸主动脉环张力,观察他克莫司对去甲肾上腺素诱导收缩的胸主动脉血管环的舒张作用,并观察伊比蝎毒素(选择性大电导钙离子激活的钾离子通道抑制剂)和雷诺定(Ryanodine,肌浆网钙离子释放抑制剂)对他克莫司舒张曲线的影响。结果:他克莫司对去甲肾上腺素(NE1.0×10-6 mol·L-1)预收缩有内皮和去内皮大鼠胸主动脉环均有显著地舒张作用,且非内皮依赖性途径在他克莫司对血管的舒张作用中起着重要作用,他克莫司对NE预收缩的去内皮大鼠胸主动脉环的舒张作用,可被雷诺定(10μmol·L-1)和iberiotoxin(100 nmol·L-1)抑制,分别从(17.41±1.94)%降至(12.38±1.17)%(雷诺定孵育前后比较,P<0.05,n=7)和(16.69±2.66)%降至(10.46±1.17)%(iberiotoxin孵育前后比较,P<0.05,n=7)。结论:他克莫司对血管的舒张作用主要是通过雷诺定受体引起钙火花的释放,从而激活大电导钙离子激活的钾离子通道(BK通道)开放引起的。
Objective: To investigate the diastolic effect of tacrolimus on thoracic aorta and its mechanism. Methods: The tension of thoracic aorta was measured by multi-channel physiology recorder. The relaxation of tacrolimus to noradrenalin-induced contraction of thoracic aortic rings was observed. The effects of icteric toxin (selective large conductance calcium Ion-activated potassium channel inhibitor) and Ryanodine (sarcoplasmic reticulum calcium release inhibitor) on tacrolimus diastolic curve. RESULTS: Tacrolimus had a significant relaxation effect on the thoracic aorta rings of endothelium and endothelium in rats with NE1.0 × 10-6 mol·L-1 precontraction, and no endothelium-dependent Pathway plays an important role in vasodilation of tacrolimus. The relaxation effect of tacrolimus on NE precontracted thoracic aorta ring in endothelium rats may be inhibited by Reynolds (10μmol·L -1) and (17.41 ± 1.94)% to (12.38 ± 1.17)% (before and after reynoldine treatment, respectively, P <0.05, n = 7) and (16.69 ± 2.66)% when compared with iberiotoxin (100 nmol·L-1) To (10.46 ± 1.17)% (before and after iberiotoxin incubation, P <0.05, n = 7). CONCLUSION: The vasodilating effect of tacrolimus is mainly caused by the release of calcium spark through Reynoldine receptor, which activates the opening of potassium channel (BK channel) activated by large conductance calcium ion.