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-