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  • Oral presentation
  • Open Access

Transgenic mice with a NO-insensitive soluble guanylate cyclase

  • 1Email author,
  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
BMC Pharmacology20077(Suppl 1):S16

https://doi.org/10.1186/1471-2210-7-S1-S16

Published: 25 July 2007

Keywords

  • Testosterone
  • Transgenic Mouse
  • Cardiac Function
  • Mutant Mouse
  • Vascular Injury

In order to distinguish between the physiological and pathogenic role of heme-dependent activation of sGC at one hand, and basal activity or heme-independent activation at the other hand, we generated knock-in mice with a H105F mutation of the beta1 subunit of sGC. These mice might furthermore be a good model for pathological situations in which the heme is functionally inactive due to oxidation, as has been suggested to be the case in a number of cardiovascular pathologies.

We observed that the mutant mice were viable, although they had a reduced life span and displayed growth retardation. They present a number of gastro-intestinal abnormalities as well as hypertension. Their response to NO donor compounds and NOS inhibition is altered but not absent. These results will be compared with those obtained in sGCalfa1-/- mice, showing testosterone dependent gender specific hypertension, altered cardiac function, altered responses to inhaled NO and to vascular injury.

Authors’ Affiliations

(1)
Ghent University and VIB, Ghent, Belgium

Copyright

© Brouckaert et al; licensee BioMed Central Ltd. 2007

This article is published under license to BioMed Central Ltd.

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