Genetic disruption of all NOSs caused metabolic syndrome, hypoadiponectinemia, hyper-low-density-lipoprotein (LDL)-emia, coronary adventitial mast cell infiltration, and vascular dysfunction. Those factors could contribute to the pathogenesis of spontaneous MI. Importantly, longterm pharmacological blockade of the angiotensin II type 1 (AT1) receptor significantly reduced the incidence of MI, along with amelioration of those risk factors. It is therefore possible that the AT1 receptor pathway is involved in its molecular mechanism [62].
