Bendall et al.20 reported a role for nNOS in the depressed β-adrenergic reserve of post-infarction rats whereas Sun et al.21 showed an increase in S-nitrosation of the L-type Ca2+ channel following ischemia/reperfusion, resulting in a reduction in Ca2+ entry and SR Ca2+ loading that was more accentuated in female mice and dependent on both nNOS and eNOS activity. Here, NOS1 is linked to infarction.