雌激素通过KATP通道影响大鼠肠系膜动脉的反应性

目的: 观察雌激素对大鼠肠系膜动脉平滑肌ATP敏感性钾离子通道 (K_ATP 通道)mRNA表达的影响,探讨K_ATP通道在雌激素调节大鼠肠系膜血管反应性中的作用。方法: 雌性SD大鼠48只,体重(100±10) g,随机分为假手术组(sham)、卵巢切除组(Ovx)和卵巢切除后补充雌激素组(Ovx +E)。采取实时荧光定量PCR检测大鼠肠系膜动脉中K_ATP通道mRNA的表达;观察各组大鼠肠系膜动脉对去甲肾上腺素(NE)升压效应的反应性。结果: 与sham组相比,Ovx组大鼠肠系膜动脉K_ATP 通道的Kir6.1及SUR2B亚单位mRNA表达减少(P<0.05),而Ovx+E组则表达增加(P<0.05)。与sham组相比,Ovx组大鼠的血管反应性明显增加(P<0.05),Ovx+E组无明显差异。给予K_ATP通道阻滞剂格列本脲后,sham组和Ovx+E组的动脉反应性增加(P<0.05),Ovx组无明显变化(P>0.05),此时3组间比较无明显差异(P>0.05)。结论: 雌激素可能通过上调肠系膜动脉平滑肌细胞K_ATP通道的表达来降低动脉对去甲肾上腺素升压效应的反应性。

Estrogen affects reactivity of rat mesenteric artery through ATP-sensitive potassium channel

AIM: To observe the expression of ATP-sensitive potassium (K_ATP) channel mRNA in mesenteric artery smooth muscle of rats with estrogen administration, and to evaluate the role of K_ATP channel in the effects of estrogen on the reactivity of mesenteric artery in rats. METHODS: Forty-eight female Sprague-Dawley rats, weighing (100?10) g, were randomly divided into 3 groups: sham operation (sham) group, ovariectomy (Ovx) group and ovariectomy with estrogen administration (Ovx+E) group. The mRNA expression of K_ATP subunits in mesenteric artery smooth muscle was detected by quantitative real-time PCR. Artery reactivity in the rats was observed by norepinephrine-induced pressor response. RESULTS: Compared with sham group, the mRNA expression of Kir6.1 and SUR2B was significantly decreased in Ovx group (P<0.05), but increased in Ovx+E group (P<0.05). Compared with sham group and Ovx+E group, the pressor response induced by norepinephrine in the rats were enhanced in Ovx group (P<0.05). No significant difference between sham group and Ovx+E group was observed. After administered with glibenclamide (a K_ATP channel blocker), the pressor response induced by norepinephrine was enhanced in sham group and Ovx +E group, and no changes in Ovx group. Meanwhile, no difference among the 3 groups was found. CONCLUSION: Estrogen up-regulates the expression of K_ATP channel subunits, which may be involved in estrogen-reduced pressor response to norepinephrine.