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血管利钠肽减弱去甲肾上腺素对心肌生长的刺激作用X(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
1999年第3期
页码:
145-148
栏目:
论著
出版日期:
1999-05-01

文章信息/Info

Title:
Use of vasonatr in peptide in the attenuation of norep inephine-induced growth-promoting effects on cardiac myocytes
作者:
于 军1　董明清1　吕顺艳1　朱妙章1　臧益民1　冯华松2　商立军1　施溥涛3
第四军医大学　1生理学教研室　西安710032　2唐都医院呼吸科　3中国科学院上海生物化学研究所
Author(s):
Yu Jun1;  Dong Mingqing1;  Lu Shunyan1;  Zhu Miaozhang1;  Zang Yimin1;  Feng Huasong2;  Shang Lijun1;  Shi Putao3
1Department of Physiology, Fourth Military Medical University, Xi′an 710032　2Department of Respiratory Disease, Tangdu Hospital, 3Shanghai Biochemistry Institute of Chinese Academy of Sciences
关键词:
血管利钠肽　去甲肾上腺素　心肌细胞　cGMP　cAMP
Keywords:
vasonatrin peptide　　norepinephine　　cardiac myocytes　　cGM P　　cAM P
分类号:
-
DOI:
-
文献标识码:
-
摘要:
本实验目的在于研究血管利钠肽(VNP)对去甲肾上腺素(NE)促心肌生长作用的影响,并对其机制进行探讨。分离、培养乳鼠心肌细胞,完全随机分为三组:对照组、NE组和VNP+ NE组。以MTT法和总蛋白含量测定法观察各组细胞的生长情况。进而采用放射免疫方法研究了VNP 对细胞内cGMP,cAMP水平的影响。结果发现:NE(10-7mol/L～10-5mol/L) 可以使培养的乳鼠心肌细胞MTT OD值显著升高(P<0.05 vs 对照组),并且具有剂量依赖性。VNP(10-7mol/L)可以显著降低NE(10-6mol/L)刺激的心肌细胞MTT OD值和细胞内总蛋白含量(P<0.05 vs NE组)。对照组和NE组细胞内cGMP,cAMP水平无显著差异, 而VNP(10-7mol/L)能升高细胞内cGMP水平,降低cAMP水平(P<0.05 vs对照组、NE组)。提示VNP能减弱NE对心肌生长的刺激作用, 其机制可能与cGMP, cAMP等信号转导分子有关。
Abstract:
This study tested the hypothesis that vasonatrin peptide(VNP) might attenuate the growth-promoting effects of norepinephine(NE)on cardiac myocytes cultured from neonatal rats.The cultured cardiac myocytes were divided randomly into three groups : control group , NE group and VNP+ NE group. The growth of cardiac myocytes was measured by means of MTT and protein content assessment. Furthermore, the effect of VNP on the intracellular level of cGMP and cAMP was measured by the means of radioimmunoassay. We found that NE (10-7mol/L～10-5mol/L)significantly increased the MTT OD value of cardiac myocytes(P<0.05 vs control group) in a dose dependent manner, and that VNP (10-7mol/L)decreased MTT OD value and the intracellular protein content in cardiac myocytes (P<0.05 vs NE group). VNP (10-7mol/L)increased the intracellular level of cGMP but decreased that of cAMP (P<0.05 vs control and NE groups). These findings indicate that VNP can attenuate the NE-induced growth-promoting effectes in cardiac myocytes, which may be due to the changes of cGM P and cAMP.

参考文献/References

［1］Galderone A , Thaik CM , Takahashi N , et al. Nitric oxide,atrial natriuretic peptide, and cyclic GMP inhibit the growth-promoting effects of norepinephine in cardiac myocytes and fibroblasts. J Clin Invest, 1998; 101 (4) : 812.

［2］Wei CM , Kim CH, Miller VM , et al. Aunique synthetic natriuretic and vasorelaxing peptide. J Clin Invest , 1993; 92:2048.

［3］冯华松, 臧益民, 朱妙章, 等. 血管利钠肽对大鼠肺动脉的舒张作用及机理. 心功能杂志, 1998; 10 (2) : 69.

［4］Cao L , Gardner DG. Natriuretic peptides inhibit DNA synthesis in cardiac fibroblasts. Hypertension, 1995; 25: 227．

［5］Levin ER. Natriuretic peptide C-receptor: more than a clearance receptor. Am J Physiol, 1993; 264: E483.

［6］Liu QY, Karpinskl E, Pang PKT. The L-type calcium channel current is increased by alpha-1 adrenoceptor activation in neonatal rat ventricular cells. J Pharmacol Exp Ther , 1994;271: 935.

［7］ Dempsey EC, McMurtry IF, O ′Brien RF. Protein kinase C activation allows pulmonary artery smooth muscle cells to proliferate to hypoxia. Am J Physiol, 1991; 260: L 136.

［8］ Tohse N , Nakaya H, Takeda Y, et al. Cylic GMP mediated inhibition of L-type Ca2+ channel by the human natriuretic.

［9］Mery RF, Lohmann SM , Walter U , et al. Ca2+ current is regulated by cyclic GMP-dependent protein kinase in mammalian cardiac myocytes. Proc. Natl Acad Sci USA , 1991; 88: 1197.

备注/Memo

备注/Memo:
(收稿19998-11-11　修回1999-05-10)国家自然科学基金资助项目 No.39770317
更新日期/Last Update: 1999-05-01