自发性高血压大鼠冠状动脉的收缩功能变化

Contractile Function of Coronary Arteries in Spontaneously Hypertensive Rats

目的探讨自发性高血压大鼠冠脉收缩力与正常大鼠的差异。方法自发性高血压大鼠(SHR)和Wistar成年大鼠,在显微镜下,操作取出冠状动脉,制备1.8~2.0mm长的离体冠状动脉环,经血管张力仪测定动脉环的张力变化。研究不同激动剂诱导冠状动脉收缩的变化。结果发现给予5-羟色胺(5-HT)、血栓素A2类似物(U46619)、内皮素-1(ET-1)均可诱导冠状动脉浓度依赖性收缩;且L-型钙通道(Cav1.2)阻断剂硝苯地平(Nifedipine)(1μmol·L^(-1))孵育后,明显抑制不同激动剂诱导血管收缩张力(P<0.05);此外,与对照组Wistar大鼠相比,SHR组给予不同激动剂诱导的冠状动脉收缩均明显较低(P<0.05);且硝苯地平(1μmol·L^(-1))孵育后,实验组诱导冠状动脉收缩较对照组明显下降(P<0.05)。结论与Wistar大鼠相比,SHR大鼠冠状动脉的收缩反应性显著减弱,可能与L型该通道介导的收缩减弱有关。

Objective To investigate the difference in coronary constriction between spontaneously hypertensive rats and normal rats.Methods The coronary arteries were removed from adult spontaneously hypertensive rats and normal Wistar rats under microscope to prepare the coronary artery rings with a length of 1.8-2.0 mm.The arterial ring tension was determined by tensiometer.The changes in coronary artery constriction were studied by using different agonists.Results The treatment with 5-hydroxytryptamine(5-HT),thromboxane A2 analogue U46619 or endothelin-1(ET-1)induced a concentration-dependent contraction in coronary arteries.The blood vessel contraction tension was significantly decreased after incubation with L-type calcium channel(Cav1.2)blocker nifedipine(1μmol·L-1)(P<0.05).Compared with normal Wistar rats,agonists-induced coronary constriction was markedly reduced in spontaneously hypertensive rats,especially after incubation with nifedipine(1μmol·L-1)(P<0.05).Conclusion Compared with normal Wistar rats,spontaneously hypertensive rats show significant decrease in the contractility of coronary artery,which may be related to the attenuation of L-type calcium channel mediated contraction.