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Cardiac overexpression of beta(2)-adrenergic receptors (beta(2)ARs) in male mice (MTG4) results in increased contractility and increased ischemic injury. Considering recent clinical data indicating that premenopausal women are protected from cardiovascular injury, we assessed the consequences of beta(2)AR overexpression in females (FTG4). Since protection in females is mediated via estrogen, which activates endothelial and inducible nitric oxide synthases (eNOS and iNOS) we also examined the role of NOS in ischemia/reperfusion injury in male and female TG4 and wild-type (WT) mice.

Male and female mice overexpressing the β2-adrenergic receptor exhibit differences in ischemia/reperfusion injury: role of nitric oxide