AngII and NE infusion produced similar pathologies in PAI-1−/− mice after 1 and 4 weeks of infusion, indicating that hemodynamic stress itself, rather than hormone-specific signaling, drives the phenotype, paralleling a report of increased cardiac fibrosis in cardiomyocyte-specific PAI-1−/− mice after transverse aortic constriction (39). This evidence concerns the gene AGT and fibrosis.