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大鼠心脏中心房钠尿肽(ANP)信使核糖核酸与ANP的同步检测——自发性高血压大鼠(SHR)左心房中ANP合成与分泌优先增加的证据

Simultaneous measurement of atrial natriuretic polypeptide (ANP) messenger RNA and ANP in rat heart--evidence for a preferentially increased synthesis and secretion of ANP in left atrium of spontaneously hypertensive rats (SHR).

作者信息

Arai H, Nakao K, Saito Y, Morii N, Sugawara A, Yamada T, Itoh H, Shiono S, Mukoyama M, Ohkubo H

机构信息

Department of Medicine, Kyoto University School of Medicine, Japan.

出版信息

Biochem Biophys Res Commun. 1987 Oct 14;148(1):239-45. doi: 10.1016/0006-291x(87)91101-6.

DOI:10.1016/0006-291x(87)91101-6
PMID:2960324
Abstract

Tissue levels of atrial natriuretic polypeptide (ANP) messenger RNA (ANPmRNA) and ANP in the rat heart were measured simultaneously. In Wistar rats, ANPmRNA of the same size (approximately 0.95 kbp) was detected in all four chambers of the rat heart. The ANPmRNA level was the highest in the right atrium, and the left atrial level was slightly lower than the right atrial level. Ventricular levels were more than two orders of magnitude lower than atrial levels. Tissue ANP concentrations of four chambers were roughly parallel to ANPmRNA levels. In spontaneously hypertensive rats (SHR) with the elevated plasma ANP level, the ANPmRNA level in the left atrium was substantially increased. The left/right ratio of atrial ANPmRNA level in SHR (150%) was higher than that in control Wistar Kyoto rats (WKY) (90%). In contrast, the left/right ratio of atrial ANP concentration was decreased in SHR (44%) compared with that in WKY (84%). The ratio of ANP to ANPmRNA levels in the left atrium of SHR was about three times smaller than that in the right atrium of SHR, and those in bilateral atria of WKY. These results indicate that the biosynthesis and secretion of ANP from the left atrium is preferentially increased in SHR. Thus, simultaneous determination of ANPmRNA and ANP levels is a refined strategy of investigation for the biosynthesis, storage and secretion of ANP.

摘要

同时测定了大鼠心脏中的心钠素(ANP)信使核糖核酸(ANPmRNA)和ANP的组织水平。在Wistar大鼠中,在大鼠心脏的所有四个腔室中均检测到相同大小(约0.95千碱基对)的ANPmRNA。ANPmRNA水平在右心房最高,左心房水平略低于右心房水平。心室水平比心房水平低两个数量级以上。四个腔室的组织ANP浓度大致与ANPmRNA水平平行。在血浆ANP水平升高的自发性高血压大鼠(SHR)中,左心房中的ANPmRNA水平显著增加。SHR中心房ANPmRNA水平的左/右比率(150%)高于对照Wistar Kyoto大鼠(WKY)(90%)。相反,与WKY(84%)相比,SHR中心房ANP浓度的左/右比率降低(44%)。SHR左心房中ANP与ANPmRNA水平的比率约为SHR右心房以及WKY双侧心房的三分之一。这些结果表明,在SHR中,左心房ANP的生物合成和分泌优先增加。因此,同时测定ANPmRNA和ANP水平是研究ANP生物合成、储存和分泌的一种精细策略。

相似文献

1
Simultaneous measurement of atrial natriuretic polypeptide (ANP) messenger RNA and ANP in rat heart--evidence for a preferentially increased synthesis and secretion of ANP in left atrium of spontaneously hypertensive rats (SHR).大鼠心脏中心房钠尿肽(ANP)信使核糖核酸与ANP的同步检测——自发性高血压大鼠(SHR)左心房中ANP合成与分泌优先增加的证据
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引用本文的文献

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Atrial Natriuretic Peptide: Structure, Function, and Physiological Effects: A Narrative Review.心房利钠肽:结构、功能及生理效应:一篇叙述性综述
Curr Cardiol Rev. 2021;17(6):e051121191003. doi: 10.2174/1573403X17666210202102210.
2
Chronic blockade of endogenous atrial natriuretic polypeptide (ANP) by monoclonal antibody against ANP accelerates the development of hypertension in spontaneously hypertensive and deoxycorticosterone acetate-salt-hypertensive rats.用抗心钠素单克隆抗体对内源性心钠素进行慢性阻断,可加速自发性高血压大鼠和醋酸脱氧皮质酮-盐性高血压大鼠高血压的发展。
J Clin Invest. 1989 Jul;84(1):145-54. doi: 10.1172/JCI114134.
3
Increased secretion of atrial natriuretic polypeptide from the left ventricle in patients with dilated cardiomyopathy.
扩张型心肌病患者左心室心房利钠多肽分泌增加。
J Clin Invest. 1989 Jan;83(1):46-51. doi: 10.1172/JCI113883.
4
A quantitative 'in-situ' hybridization method using computer-assisted image analysis. Validation and measurement of atrial-natriuretic-factor mRNA in the rat heart.一种使用计算机辅助图像分析的定量“原位”杂交方法。大鼠心脏中的心钠素mRNA的验证与测量。
Biochem J. 1989 Oct 1;263(1):121-7. doi: 10.1042/bj2630121.
5
Effects of the administration of thyroid hormone on the plasma levels of atrial natriuretic peptides and on atrial myoendocrine cells in the rat: an immunochemical, ultrastructural, and stereological study.甲状腺激素给药对大鼠血浆心房利钠肽水平及心房肌内分泌细胞的影响:一项免疫化学、超微结构及体视学研究。
J Endocrinol Invest. 1992 Nov;15(10):727-34. doi: 10.1007/BF03347641.