我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

血管钠肤抑制异丙肾上腺素对心肌细胞收缩的增强作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2004年第3期
页码:
204-208
栏目:
实验研究
出版日期:
2004-05-01

文章信息/Info

Title:
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
第四军医大学:1.生理学教研室，2.西京医院老年病科，陕西 西安，710032
Author(s):
Guo Hai-tao1; ZHU Miao-zhang1; ZHANG Rong-huai2; BI Hui1; Lu Shun-yan1
1.Department of Physioloy,2.Geriatrics of Xijing Hospital，Fourth Military Medical University, Xi'an,Shaanxi 710032,China
关键词:
血管钠肤; 心肌细胞; cGMP; 镁蓝; 收缩福度; 收缩
Keywords:
vasonatrin peptide; cardiac myocytes; cyclic GMP; methylene blue; twitch amplitude; contractio
分类号:
Q463
DOI:
-
文献标识码:
A
摘要:
目的:研究血管钠肤(VNP)对心肌细胞收缩的作用及其机制，观察HS-142-1,8-Br-cGMP和镁蓝(methylene blue,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:10-10,10-9,10-8,10-7,10-6 mol/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) %, (26±2)%、(60±5) %,(153±4)%和(312±7)%。此效应可被普蔡洛尔(10-6 mol/L)所阻断。10-10,10-9,10-8,10-7,10-6 mol/L VNP可剂量依赖性地抑制Iso(10-8 mol/L)引起的心肌细胞收缩幅度的升高，与Iso(10-8 mol/L)相比较分别减弱(99±3)%、(95±2) %,(84±6)%,(66±3)%和(61±3)%, 8-Br-cGMP(10-7-10-3mol/L)也可剂量依赖性地抑制Iso(10-8 mol/L)引起心肌细胞收缩的增强。钠尿肤鸟昔酸环化酶(guanylate cyclase,GC)受体的特异性阻断剂HS-142-1(2 * 10-5 mol/L)使VNP的作用几乎完全消失。MB是GC的抑制剂，10-5 mol/LMB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-142-1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作用于心肌细胞的钠尿肤GC受体，通过升高细胞内cGMP水平发挥降低细胞收缩的作用。
Abstract:
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 beta-adrenergic bloker, 1 μmol/L). The effect of Iso (10-6 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 X 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 ainpitude 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.

参考文献/References

[1] Burger AJ, Burger MR, Aronson D. New therapies for the treatment of congestive heart failure[J].Drugs Today,2002,38(1): 31-48.

[2] Werdan K. Cytokines and heart disease,attemptatan update[J]. Med Klin,1997,92(7):432-438.

[3] Marei HE. Fine structural and immunohistochemical localization of cardiac hormones(ANP) in the right atrium and hypothalamus of the white rat[J]. Eur J Morphol, 2002,40(1):37-41.

[4] Rybalkin SD, Yan C Bornfeldt KE, et al. Cyclic GMP phosphodiesterases and regulation of smooth muscle function[J].Circ Res,2003,93(4):280-291.

[5] Wei CM ，Kim CH, Miller VM, et al. Vasonatrin peptides A unique synthetic natriureti can dvasorelaxing peptide[J].J Clin Invest, 1993,92(4):2048-2052.

[6] Yu J，Zhu MZ, Wei GZ, et al. Vasorelaing role of vasonatrin peptide in human intramammary artery in vitro[J].Acta Physiol Sin, 2003,55(2):187-190(Chinese,English abstract).

[7] Nir A, Zhang DF, Fixler R,et al. C-type natriuretic peptide has a negative inotropic effect on cardiac myocytes[J].Eur J pharmacol, 2001,412(3):195-201.

[8] Pukki KJ. Cytokines and cardiomycyte death[J]. Ann Med,1997 ,29(4):339-343.

[9] Kelly RA, Smith TW. Cytokines and cardic contractile function[J]. Circulation,1997,95(4):778-781.

[10]Morishita R, Gibbons GH, Pratt RE, et al. Autocrine and paracrine effects of atrial natriuretic peptide gene transfer on vascular smooth muscle and endothelial cellular growth[J].J Clin Investig,1994,94(2):824-829.

[ll]Kishimoto R, Rossi K, Garbers L. A genetic model provides evidence that the receptor for atrial natriuretic peptide(guanylyl cyclase-A)inhibits cardiac ventricular myocyte hypertrophy[J]. Proc Natl Acad Sci USA,2001,98(5):2703-2706.

[12]Hansson M, Barroso C, Gulbenkian S, et al. occurrence of binding sites for[125I] ANP in the myocardium butnot in Purkinje fibers of the bovine heart[J].Cell Tissue Re,1997,290(3): 669-673.

[13]Ryu SY, Lee SH, Isenberg G, et al. Monitoring of ANP secretion from single atrial myocytes using densitometry[J]. Pflugers Arch,2002,444(4):568-577.

[14] Kaganovsky E,Belkin V,Barhum Y,et al.Occurrence and distribution of atrialn atriuretic peptide-containing cells in the left ventricle of hypertensive rats. Effect of antihypertensive treatment [J]. Cell Tissue Res, 2001,303(1):57-67.

[15]Spurgeon HA, Stern MD, Baartz G,et al. Simultaneous measurement of Ca2+，contraction,and potential in cardiacmyocytes [J].Am J Physiol,1990,258(2 Pt 2):H574-H586.

备注/Memo

备注/Memo:
收稿日期：2002-12-30
更新日期/Last Update: 2004-05-01