葛根素对慢性低O_2高CO_2大鼠肺动脉及右心室尾加压素Ⅱ受体的影响

目的探讨葛根素对慢性低氧高二氧化碳大鼠肺动脉及右心室尾加压素Ⅱ(UⅡ)受体(UT)表达的影响。方法SD大鼠30只分为:正常对照组(NC)、低氧高二氧化碳组(HH)、低氧高二氧化碳加葛根素组(HP)。放免法测定血浆UⅡ的含量,放射性配基结合法测定大鼠肺主动脉组织质膜及右心室肌浆膜上UT受体的结合率,图像分析、组织原位杂交技术等方法观察葛根素对慢性低氧高二氧化碳大鼠肺细小动脉UT mRNA的影响。结果①平均肺动脉压(mPAP)、右心室/左心室和室间隔的重量比(RV/LV+S):HH组较NC组明显升高(P<0.01),HP组明显低于HH组(P<0.01);各组间平均颈动脉压(mCAP)差异无显著性(P>0.05)。②右心室及肺动脉UT受体的最大结合率(Bmax):HH组较NC组增加(P<0.01),HP组则低于HH组(P<0.01);UT受体亲和力(Kd值)及血浆UⅡ浓度3组间差异无显著性(P>0.05)。③三级肺细小动脉UT mRNA的表达水平:HH组较NC组均上调(P<0.01),HP组均明显低于HH组(P<0.05)。结论葛根素减轻大鼠慢性低O2高CO2性肺动脉高压及右心室肥大的作用可能与其抑制肺动脉及右心室UT的表达有关。

Effects of puerarin on urotensin Ⅱ receptor in pulmonary arteries and right ventricle of chronic hypoxia-hypercapnia rats

Aim To investigate the effects of puerarin on the urotensin Ⅱ receptor(UT) in pulmonary arteries(arterials)and right ventricle of chronic hypoxia-hypercapnia rats.Methods Thirty male Sprague-Dawley rats were randomly divided into three groups,control group(NC),hypoxia-hypercapnia group(HH),hypoxia-hypercapnia+puerarin group(HP).Plasma UⅡ cocentration was measured with radio-immunity method.UⅡ receptor binding sites of pulmonary arteries sarcolemmaand myocardial sarcolemma were determined using radioligand assay.UT mRNA in various grades of pulmonary arterioles were measured by in situ hybridization.Results ① mPAP and RV/LV+S were much higher in HH group than those of NC group(P<0.01),while lower in HP group than those of HH group(P<0.01).Differences of mCAP were not found among three groups(P>0.05);② UT(B_(max)) of HH group was higher than that of NC group(P<0.01),and lower in HP group than that of HH group(P<0.01).No difference existed among each group in the affinity to UⅡand concentration of UⅡ in plasma(P>0.05);③ Expression of UT mRNA in three grades of pulmonary arterioles were upregulated in HH group compared with NC group(respectively,P<0.01),while lower in HP group than HH group(respectively,P<0.05).Conclusion Puerarin inhibits the expression of UT in pulmonary arteries and right ventricle,and improves pulmonary hypertension and right ventricular hypertrophy induced by chronic hypoxia-hypercapnia in rats.