Conditional neuronal nitric oxide synthase overexpression impairs myocardial contractility

Natalie Burkard, Adam G. Rokita, Susann G. Kaufmann, Matthias Hallhuber, Rongxue Wu, Kai Hu, Ulrich Hofmann, Andreas Bonz, Stefan Frantz, Elizabeth J. Cartwright, Ludwig Neyses, Lars S. Maier, Sebastian K G Maier, Thomas Renné, Kai Schuh, Oliver Ritter

    Research output: Contribution to journalArticlepeer-review


    The role of the neuronal NO synthase (nNOS or NOS1) enzyme in the control of cardiac function still remains unclear. Results from nNOS mice or from pharmacological inhibition of nNOS are contradictory and do not pay tribute to the fact that probably spatial confinement of the nNOS enzyme is of major importance. We hypothesize that the close proximity of nNOS and certain effector molecules like L-type Ca-channels has an impact on myocardial contractility. To test this, we generated a new transgenic mouse model allowing conditional, myocardial specific nNOS overexpression. Western blot analysis of transgenic nNOS overexpression showed a 6-fold increase in nNOS protein expression compared with noninduced littermates (n=12; P
    Original languageEnglish
    Pages (from-to)e32-e44
    JournalCirculation research
    Issue number3
    Publication statusPublished - Feb 2007


    • Conditional overexpression
    • Contractility
    • Contraction coupling
    • Excitation
    • nNOS


    Dive into the research topics of 'Conditional neuronal nitric oxide synthase overexpression impairs myocardial contractility'. Together they form a unique fingerprint.

    Cite this