Todorov, V and Gess, B and Godecke, A and Wagner, C and Schrader, J and Kurtz, A (2000) Endogenous nitric oxide attenuates erythropoietin gene expression in vivo. PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 439 (4). pp. 445-448. ISSN 0031-6768,
Full text not available from this repository.Abstract
This study aimed to investigate the role of endogenous nitric oxide (NO) in erythropoietin (EPO) gene expression in mice in vivo. For this purpose EPO mRNA was semiquantitated by ribonuclease protection assay in livers and kidneys of three groups of mice: wild-type (wt), endothelial NO-synthase (NOS) knockout mice (eNOS-/-), and wt treated with the NOS inhibitor N-G-nitro-L-arginine methyl ester (50 mg.kg(-1).day(-1)) for 4 days (wt+L-NAME). EPO gene expression was stimulated by normobaric hypoxia (8% O-2) Or by 0.1%, carbon monoxide (CO) inhalation for 4 h each, or by intraperitoneal injection of 60 mg/kg cobaltous chloride (CoCl2) for 6 h. Renal EPO mRNA in wt increased 12-, 40-, and 13-fold over normoxic levels in response to hypoxia, CO and CoCl2 respectively. EPO mRNA was detectable in the livers only after CO exposure. Renal and hepatic EPO gene expression in wt+L-NAME appeared moderately increased relative to wt with a maximal 2.5-fold enhancement after CO exposure. EPO mRNA levels in eNOS-/- mirrored those of wt+L-NAME, but the effects were less prominent. Our data suggest that endogenous NO attenuates EPO gene expression in mice. This effect is dependent on the rate of EPO gene induction.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | HYPOXIA; DONORS; endothelial NO-synthase; erythropoietin mRNA; hypoxia; knockout mice; N-G-nitro-L-arginine methyl ester |
| Subjects: | 500 Science > 590 Zoological sciences |
| Divisions: | Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Armin Kurtz |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 21 May 2021 07:40 |
| Last Modified: | 21 May 2021 07:41 |
| URI: | https://pred.uni-regensburg.de/id/eprint/42869 |
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