As systemic hypoxia and hypertension occurred and lasted, increased workload imposed the remodeling into pathological development, as shown by persistently augmented HIF-1α activation, calcineurin-NAFT (nuclear factor of activated T-cells) signaling, inflammation, and fibrosis [8,10], as well as by upregulation of ANP, MHC-β, and oxidative stress, in the present study. This evidence concerns the gene HIF1A and hypertensive disorder.