In animals, HO-1−/− mice reportedly had the same blood pressure as controls suggesting HO-1 is not involved in the maintenance of blood pressure under physiological conditions [261]; nevertheless, unilateral kidney clamping in HO-1−/− animals induced more severe hypertension and cardiac hypertrophy than in heterozygous or HO-1+/+ mice, with extensive ischemic injury at the corticomedullary junction [261]. This evidence concerns the gene HMOX1 and hypertensive disorder.