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学科主题: 临床医学
题名:
Potentiated response to adrenomedullin in myocardia and aortas in spontaneously hypertensive rat
作者: Pan, CS; Jiang, W; Wu, SY; Zhao, J; Pang, YZ; Tang, CS; Qi, YF
关键词: spontaneously hypertensive rats ; adrenomedullin ; calcitonin receptor-like receptor ; receptor activity-modifying proteins ; cAMP
刊名: BASIC RESEARCH IN CARDIOLOGY
发表日期: 2006-05-01
DOI: 10.1007/s00395-005-0583-y
卷: 101, 期:3, 页:193-203
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems
研究领域[WOS]: Cardiovascular System & Cardiology
关键词[WOS]: RECEPTOR-LIKE RECEPTOR ; LEFT-VENTRICULAR HYPERTROPHY ; GENE-EXPRESSION ; HEART-FAILURE ; ENDOTHELIAL-CELLS ; SYSTEM ; PEPTIDE ; SECRETION ; COMPLEXES ; LIGAND
英文摘要:

Adrenomedullin (AM) is a multifunctional regulatory peptide, and endogenous AM is an important factor in regulating cardiovascular and renal homeostasis as a potent cardio-reno-protective factor. To illustrate the protective mechanism of adrenomedullin (AM) on the cardiovascular system by observing (1) the changes in mRNA and protein levels of AM and its receptor-calcitonin receptor-like receptor (CL) and receptor activity-modifying proteins (RAMPs)-in myocardia and aortas of spontaneously hypertensive rats (SHRs) and (2) the response of cardiovascular tissue to AM. The AM content and cyclic adenosine monophosphate (cAMP) production in myocardia and aortas were measured in SHRs and Wistar Kyoto (WKY) rats (11-week-old) by radioimmunoassay (RIA). The mRNA levels of brain natriuretic peptide (BNP), AM, CL, RAMP1, -2, -3 were determined by semi-quantitative RTPCR. Protein levels of CL, RAMP1, -2, -3 were assayed by Western blotting. SHRs had severe hypertension, and the tail-blood pressure was 76.7% higher, the ratio of heart weight to body weight (heart coefficient) 45.5% higher, and the BNP gene expression 4.5-fold higher than that of WKY rats (all p < 0.01). The AM-ir content in plasma, myocardia and aortas of SHRs increased by 42.5%, 68.3% and 80.4%, respectively (all p < 0.01) compared with WKY rats. Furthermore, the mRNA levels of AM, CL, RAMP1, RAMP2 and RAMP3 were elevated by 46% (p < 0.01), 62% (p < 0.05), 51.2% (p < 0.01), 41% (p < 0.01) and 54% (p < 0.01), respectively, in myocardia and by 72%, 87%, 155%, 53% and 74% (all p < 0.01), respectively, in aortas. The elevated mRNA level of CL, RAMP1 RAMP2 and RAMP3 correlated positively with that of AM mRNA in hypertrophic myocardia (r= 0.943, 0.621, 0.688 and 0.633, respectively, all p < 0.01) and aortas (r = 0.762, 0.892, 0.828 and 0.736, respectively, all p < 0.01). The protein levels of CL, RAMP1, RAMP2 and RAMP3 in myocardia and aortas of SHRs were increased compared with that of WKY rats. The response to AM was potentiated in myocardia and aortas in SHRs, and the production of cAMP was increased by 47% and 65% (both p < 0.01), respectively. AM-stimulated cAMP generation in myocardia and aortas was blocked by both AM(22-52), the specific antagonist of AM, and calcitonin gene-related peptide (CGRP)(8-37), the antagonist of the CGRP1 receptor. In myocardia and aortas of SHRs, the gene expressions and protein levels of AM, CL, RAMP1, RAMP2 and RAMP3 were increased, and the response to AM was potentiated. AM-stimulated cAMP generation in myocardia and aortas was blocked by both AM(22-52) and CGRP(8-37). The results suggest that the changes of AM and its receptors in cardiovascular tissue, and the increased response of cardiovascular tissue to AM might importantly impact the pathogenesis of hypertension.

语种: 英语
WOS记录号: WOS:000236643000001
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63586
Appears in Collections:北京大学第一临床医学院_心血管内科_期刊论文

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作者单位: 1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100083, Peoples R China
2.Yunyang Med Coll, Dept Pathophysiol, Shiyan 442000, Peoples R China
3.Peking Univ, Hosp 1, Inst Cardiovasc Dis, Beijing 100034, Peoples R China

Recommended Citation:
Pan, CS,Jiang, W,Wu, SY,et al. Potentiated response to adrenomedullin in myocardia and aortas in spontaneously hypertensive rat[J]. BASIC RESEARCH IN CARDIOLOGY,2006,101(3):193-203.
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