In deoxycorticosterone acetate-salt hypertension, arginase is also involved in its pathogenesis, and both arginase isoforms contribute to vascular endothelial dysfunction, especially ARG1 that is upregulated in the aorta of rats with deoxycorticosterone acetate-salt hypertension and associated with the elevated systolic blood pressure (BP), impaired endothelium-dependent vasorelaxation and increased vasoreactivity to constrictor stimuli [105]. This evidence concerns the gene ARG1 and Hypertension.