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Transgenic mice with a NO-insensitive soluble guanylate cyclase

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.

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Correspondence to Peter Brouckaert.

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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Brouckaert, P., Thoonen, R., Sips, P. et al. Transgenic mice with a NO-insensitive soluble guanylate cyclase. BMC Pharmacol 7 (Suppl 1), S16 (2007).

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