血管钠肽抑制异丙肾上腺素对心肌细胞收缩的增强作用  

The attenuating effects of vasonatrin peptide on the enhancement of electrically-induced twitch amplitude by isoproterenol in rat cardiac myocytes

作　　者：郭海涛[1] 朱妙章[1] 张荣怀[2] 毕辉[1] 吕顺艳[1] 

机构地区：[1]第四军医大学生理学教研室 [2]第四军医大学西京医院老年病科,陕西西安710032

出　　处：《心脏杂志》2004年第3期204-208,共5页Chinese Heart Journal

基　　金：国家自然科学基金资助项目 ( No.3 9970 3 2 7) ;陕西省自然科学基金资助项目 ( No.2 0 0 3 C2 0 2 3 )

摘　　要：目的 :研究血管钠肽 (VNP)对心肌细胞收缩的作用及其机制 ,观察 HS- 14 2 - 1、8- Br- c GMP和镁蓝 (methyleneblue,MB)对心肌细胞收缩的影响。方法 :采用单心肌细胞动缘探测技术检测细胞收缩的幅度。结果 :10 - 1 0、10 - 9、10 - 8、10 - 7、10 - 6 m ol/L Iso可剂量依赖性地引起心肌细胞收缩增强 ,与对照组相比较分别增强 (13± 3) %、(2 6± 2 )%、 (6 0± 5 ) %、(15 3± 4 ) %和 (312± 7) %。此效应可被普萘洛尔 (10 - 6 mol/L )所阻断。 10 - 1 0 、10 - 9、10 - 8、10 - 7、10 - 6 m ol/L VNP可剂量依赖性地抑制 Iso(10 - 8mol/L)引起的心肌细胞收缩幅度的升高 ,与 Iso(10 - 8mol/L)相比较分别减弱 (99± 3) %、(95± 2 ) %、(84± 6 ) %、(6 6± 3) %和 (6 1± 3) %。 8- Br- c GMP(10 - 7～ 10 - 3m ol/L)也可剂量依赖性地抑制 Iso(10 - 8mol/L)引起心肌细胞收缩的增强。钠尿肽鸟苷酸环化酶 (guanylate cyclase,GC)受体的特异性阻断剂 HS- 14 2 - 1(2× 10 - 5mol/L)使 VNP的作用几乎完全消失。MB是 GC的抑制剂 ,10 - 5mol/L MB不但使VNP的作用完全消失 ,而且增强心肌细胞收缩的效应。VNP和 HS- 14 2 - 1本身对心肌细胞收缩无显著影响。而 MB使心肌细胞收缩幅度升高。结论 :VNP作用于心肌细?AIM:To investigate the effects of vasonatrin peptide (VNP) on electrically-induced contraction, to underlie the mechanism of the effects in the cardiac myocytes, and to determine the effects of HS-142-1, 8-Br-cGMP and methylene blue(MB) on twitch ampitude in cardiac myocytes. METHODS:The twitch ampitude was measured with a video edge tracker method. RESULTS:Isoproterenol (Iso) at different levels 10 -10 ,10 -9 ,10 -8 ,10 -7 ,10 -6 mol/L augmented electrically-induced contraction dose-dependently, with the augmenting rates of (13±3)%, (26±2)%, (60±5)%, (153±4)% and (312±7)%, respectively. These effects were blocked by propranolol (an β-adrenergic bloker, 1 μmol/L). The effect of Iso (10 -8 mol/L) on twitch ampitude was attenuated in a dose-dependent manner by VNP at levels of 10 -10 ,10 -9 ,10 -8 ,10 -7 ,10 -6 mol/L, the attenuating rates being(99±3) %, (95±2) %, (84±6) %, (66±3) % and (61±3) %, respectively. 8-Br-cGMP (10 -7 ~10 -3 mol/L) aslo attenuated 10 -8 mol/L Iso-induced contraction dose-dependently. The effect of VNP on contraction was almost abolished in the presence of HS-142-1 (2×10 -5 mol/L), an antagonist of the natriuretic peptide guanylate cyclase (GC) receptors. MB (10 -5 mol/L), an inhibitor of GC, not only blocked the effect of VNP in cardiac myocytes, but also augmented electrically-induced contraction. VNP and HS-142-1 didn't significantly change the twitch ampitude in the cardiac myocytes. But MB augmented the twitch ampitude in the cardiac myocytes significantly. CONCLUSION:These results suggest that VNP attenuates twitch ampitude induced by Iso. This effect is possibly achieved by the binding of VNP with the natriuretic peptide GC receptors in the cardiac myocytes, leading to an increase in intracellular cGMP.

关 键 词：血管钠肽 心肌细胞 CGMP 镁蓝 收缩幅度 收缩 

分 类 号：Q463[生物学—生理学]