Mechanism of ANP and BNP Action on the Suppression of Aldosterone Secretion by Cultured Bovine Adrenal Glomerulosa Cells

Q4 Biochemistry, Genetics and Molecular Biology Japanese Journal of Clinical Chemistry Pub Date : 1993-09-30 DOI:10.14921/JSCC1971B.22.3_156
R. Uzawa, K. Su, Taiichiro Kobayashi, Hiroyuki Watanabe, K. Fukuchi, Y. Takagi, K. Gomi, Chang Gu Kang
{"title":"Mechanism of ANP and BNP Action on the Suppression of Aldosterone Secretion by Cultured Bovine Adrenal Glomerulosa Cells","authors":"R. Uzawa, K. Su, Taiichiro Kobayashi, Hiroyuki Watanabe, K. Fukuchi, Y. Takagi, K. Gomi, Chang Gu Kang","doi":"10.14921/JSCC1971B.22.3_156","DOIUrl":null,"url":null,"abstract":"Atrial natriuretic peptide (ANP) (10-8mol/l), brain natriuretic peptide (BNP) (10-8mol/l), the protein kinase C (PKC) inhibitors H-7 (10-5mol/l) and staurosporin (10-8mol/l) suppressed aldosterone secretion in cultured bovine adrenal glomerulosa cells by 40 to 50 % compared with untreated control cells. When cells incubated with 10-8mol/l angiotensin II (All) were also treated with ANP, BNP, or PKC inhibitors, aldosterone secretion was 50 to 60 % of that seen in untreated cells. ANP, BNP and PKC inhibitors suppressing the expression of PKC, suggested that PKC plays a role in aldosterone secretion. Our results suggest that ANP and BNP may have an unknown second messenger pathway in which the suppression of PKC is essential for the ex-","PeriodicalId":39360,"journal":{"name":"Japanese Journal of Clinical Chemistry","volume":"22 1","pages":"156-161"},"PeriodicalIF":0.0000,"publicationDate":"1993-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Japanese Journal of Clinical Chemistry","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.14921/JSCC1971B.22.3_156","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 0

Abstract

Atrial natriuretic peptide (ANP) (10-8mol/l), brain natriuretic peptide (BNP) (10-8mol/l), the protein kinase C (PKC) inhibitors H-7 (10-5mol/l) and staurosporin (10-8mol/l) suppressed aldosterone secretion in cultured bovine adrenal glomerulosa cells by 40 to 50 % compared with untreated control cells. When cells incubated with 10-8mol/l angiotensin II (All) were also treated with ANP, BNP, or PKC inhibitors, aldosterone secretion was 50 to 60 % of that seen in untreated cells. ANP, BNP and PKC inhibitors suppressing the expression of PKC, suggested that PKC plays a role in aldosterone secretion. Our results suggest that ANP and BNP may have an unknown second messenger pathway in which the suppression of PKC is essential for the ex-
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
ANP和BNP抑制培养的牛肾上腺肾小球细胞分泌醛固酮的作用机制
心房利钠肽(ANP) (10-8mol/l)、脑利钠肽(BNP) (10-8mol/l)、蛋白激酶C (PKC)抑制剂H-7 (10-5mol/l)和staurosporin (10-8mol/l)对培养的牛肾上腺肾小球细胞醛固酮分泌的抑制作用比未处理的对照组细胞降低40 ~ 50%。当细胞用10-8mol/l血管紧张素II (All)孵育时,也用ANP、BNP或PKC抑制剂处理,醛固酮的分泌量是未处理细胞的50 - 60%。ANP、BNP和PKC抑制剂抑制PKC的表达,提示PKC在醛固酮分泌中起作用。我们的研究结果表明ANP和BNP可能具有未知的第二信使途径,其中PKC的抑制对前-通路至关重要
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
Japanese Journal of Clinical Chemistry
Japanese Journal of Clinical Chemistry Biochemistry, Genetics and Molecular Biology-Clinical Biochemistry
自引率
0.00%
发文量
5
期刊最新文献
Cytokine profiles in mice with arthritis induced by anti-type II collagen monoclonal antibody plus lipopolysaccharide Assessment of renal function in pediatric medicine Metabolome Analysis by CE-MS and Application to Biosciences Bile Acids Control Lipogenesis and Energy Metabolism Na+, K+- ATPase and cardiovascular disease
×
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