Cell biology of atrial natriuretic peptide.

Blood vessels Pub Date : 1991-01-01 DOI:10.1159/000158847
C Huot, J Tremblay, P Hamet
{"title":"Cell biology of atrial natriuretic peptide.","authors":"C Huot,&nbsp;J Tremblay,&nbsp;P Hamet","doi":"10.1159/000158847","DOIUrl":null,"url":null,"abstract":"<p><p>Atrial natriuretic peptide (ANP) exhibits a wide spectrum of cardiovascular, endocrine, metabolic and renal actions. cGMP is the major mediator of ANP at the cellular level and only tissues possessing particulate guanylate cyclase appear to present ANP-induced actions. Three types of ANP receptors have recently been cloned. Two of them (A and B receptors) are homologous and contain guanylate cyclase catalytic domains. The C receptor could possibly regulate the metabolic fate of ANP. Data obtained by the radiation inactivation method suggest the presence of an inter- or intramolecular inhibitory component of nearly 90 kilodaltons that represses the catalytic activity of guanylate cyclase within its membrane environment. The mechanism of guanylate cyclase stimulation by ANP could involve this inhibitory component. Preliminary data suggest that the hyperresponsiveness of the particulate guanylate cyclase/cGMP system in hypertension occurs through modulation of the inhibitory component.</p>","PeriodicalId":9009,"journal":{"name":"Blood vessels","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000158847","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Blood vessels","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000158847","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6

Abstract

Atrial natriuretic peptide (ANP) exhibits a wide spectrum of cardiovascular, endocrine, metabolic and renal actions. cGMP is the major mediator of ANP at the cellular level and only tissues possessing particulate guanylate cyclase appear to present ANP-induced actions. Three types of ANP receptors have recently been cloned. Two of them (A and B receptors) are homologous and contain guanylate cyclase catalytic domains. The C receptor could possibly regulate the metabolic fate of ANP. Data obtained by the radiation inactivation method suggest the presence of an inter- or intramolecular inhibitory component of nearly 90 kilodaltons that represses the catalytic activity of guanylate cyclase within its membrane environment. The mechanism of guanylate cyclase stimulation by ANP could involve this inhibitory component. Preliminary data suggest that the hyperresponsiveness of the particulate guanylate cyclase/cGMP system in hypertension occurs through modulation of the inhibitory component.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
房利钠肽的细胞生物学。
心房利钠肽(ANP)具有广泛的心血管、内分泌、代谢和肾脏作用。在细胞水平上,cGMP是ANP的主要介质,只有含有颗粒鸟苷酸环化酶的组织才表现出ANP诱导的作用。最近已经克隆了三种类型的ANP受体。其中两个(A和B受体)是同源的,并且含有鸟苷酸环化酶催化结构域。C受体可能调控ANP的代谢命运。通过辐射失活方法获得的数据表明,存在近90千道尔顿的分子间或分子内抑制成分,抑制了鸟苷酸环化酶在其膜环境中的催化活性。ANP刺激鸟苷酸环化酶的机制可能与这种抑制成分有关。初步数据表明,颗粒鸟苷酸环化酶/cGMP系统在高血压中的高反应性是通过抑制成分的调节发生的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Contractile and morphologic properties of a saphenous vein after 12 years as an aortocoronary bypass graft. Effect of H-8, an isoquinolinesulfonamide inhibitor of cyclic nucleotide-dependent protein kinase, on cAMP- and cGMP-mediated vasorelaxation. Hemorheological effects of buflomedil: action on shape and functions of the human neutrophils. Norepinephrine, phentolamine and buflomedil influence on arteriolar vasomotion in the hamster skinfold preparation. Heme-dependent activation of guanylate cyclase by nitric oxide: a novel signal transduction mechanism.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1