For instance, in this lean CIH model without histological kidney damage, upon established HTN (35 days), the nonselective β-blocker carvedilol, with intrinsic anti-α1-adrenergic and antioxidant properties [34], which is a substrate of CYP1A1 [109], was not able to reverse CIH-increased BP, which has occurred with an AhR antagonist [26]. The gene discussed is CYP1A1; the disease is hypertensive disorder.