Chemical preconditioning in mice is not mediated by upregulation of nitric oxide synthase isoforms

  • Von Arnim C
  • Timmler M
  • Ludolph A
 et al. 
  • 4

    Readers

    Mendeley users who have this article in their library.
  • 8

    Citations

    Citations of this article.

Abstract

Ischemic preconditioning requires increased nitric oxide (NO) production. However, NO may also trigger delayed neuronal death cascades. The goal therefore was to investigate nitric oxide synthase (NOS) isoforms (neuronal NOS: nNOS; endothelial NOS: eNOS; inducible NOS: iNOS) with reverse transcriptase-polymerase chain reaction in hippocampal slices from control mice and slices prepared upon preconditioning in vivo (single intraperitoneal injection of 20 mg/kg body weight 3-nitropropionate (3NP)). One hour after preconditioning nNOS (108 ± 34%, mean ± SD), eNOS (93 ± 34%), and iNOS (282 ± 261%) remained at control levels. Similarly, nNos, eNOS, and iNOS stayed at control level 12, 24, and 72 h after preconditioning with 3NP. Incubation of slices, however, drastically increased iNOS (1676 ± 818, P < 0.01). We conclude that chemical preconditioning other than ischemic preconditioning may not increase potentially harmful nitric oxide synthase isoforms. © 2001 Elsevier Science Ireland Ltd.

Author-supplied keywords

  • Hippocampus
  • Hypoxia
  • Isoforms
  • Nitric oxide synthase
  • Preconditioning

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document

Authors

  • Ahmadreza DaraeiUniversity of Sistan and Baluchestan, Faculty of Science, Department of Physics

    Follow
  • C. A F Von Arnim

  • Melanie Timmler

  • Albert C. Ludolph

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free