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Brunssen, C.* ; Hofmann, A.* ; Peitzsch, M.* ; Frenzel, A.* ; Ziegler, C.G. ; Brown, N.F.* ; Weldon, S.M.* ; Eisenhofer, G.* ; Willenberg, H.S.* ; Bornstein, S.R.* ; Morawietz, H.*

Impact of aldosterone synthase inhibitor FAD286 on steroid hormone profile in human adrenocortical cells.

Horm. Metab. Res. 49, 701-706 (2017)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Inhibition of aldosterone synthase (CYP11B2) is an alternative treatment option to mineralocorticoid receptor antagonism to prevent harmful aldosterone effects. FAD286 is the best characterized aldosterone synthase inhibitor. However, to date, no study has used sensitive liquid chromatography-tandem mass spectrometry to characterize in detail the effect of FAD286 on the secreted steroid hormone profile of adrenocortical cells. Basal aldosterone production in NCI-H295R cells was detectable and 9-fold elevated after stimulation with angiotensin II. FAD286 inhibited this increase, showing a maximal effect at 10 nmol/l. Higher concentrations of FAD286 did not further reduce aldosterone concentrations, but showed a parallel reduction in corticosterone, cortisol and cortisone levels, reflecting additional inhibition of steroid-11 beta-hydroxylase (CYP11B1). Pregnenolone, progesterone and 17-OH-progesterone levels remained unaffected. In conclusion, the aldosterone synthase inhibitor FAD286 lowers angiotensin II-induced aldosterone concentrations in adrenocortical cells but the relative lack of selectivity over CYP11B1 is evident at higher FAD286 concentrations.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Aldosterone ; Steroid Hormones ; Mineralocorticoids ; Glucocorticoids ; Adrenal Cortex; Angiotensin-ii; H295r Cells; System; Receptor; Rats; 11-beta-hydroxylase; Hyperaldosteronism; Expression; Fadrozole; Nci-h295r
Sprache englisch
Veröffentlichungsjahr 2017
HGF-Berichtsjahr 2017
ISSN (print) / ISBN 0018-5043
e-ISSN 1439-4286
Zeitschrift Hormone and Metabolic Research
Quellenangaben Band: 49, Heft: 9, Seiten: 701-706 Artikelnummer: , Supplement: ,
Verlag Thieme
Verlagsort Stuttgart
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Pancreatic Islet Research (IPI)
POF Topic(s) 90000 - German Center for Diabetes Research
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-502600-007
DOI 10.1055/s-0043-113829
WOS ID WOS:000410529100009
PubMed ID 28759940
Scopus ID 85026858295
Erfassungsdatum 2017-09-29
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