Table 3.

Antioxidant therapy in hypertension.

Agents	Intervention objects	Mechanisms	Biological effects	Reference
Vitamin C	Patients with hypertension	Have a beneficial effect on vasodilation	Antagonizing the free contraction induced by norepinephrine by antioxidation	(148)
BCL6	Ang-II induced hypertensive rats	Reduces producing of ROS and cell apoptosis	Inhibits vascular smooth muscle cells proliferation, attenuating oxidative stress injury and microvascular remodeling	(149, 150)
ACEIs/ARBs	Diabetic rats or patients with coronary artery disease	Suppress the RAAS producing ROS	Effectively inhibit the activity of NADPH oxidase, improve the superoxide dismutase activity, prevent eNOS from uncoupling and enhance of NO activity	(149, 151–153)
Novel beta-blockers	Hypertensive patients	Protect endothelial function	Reduces the ROS production from inflammatory cells and the oxidation of LDL, improve endothelium dependent vasodilation performance, inhibit the activity and expression of NADPH oxidase and prevent eNOS uncoupling and promoting eNOS activity	(154–156)
CCBs	Human aortic endothelial cells	Prevent oxidized low density lipoprotein	Lower the ROS production to alleviate oxidative damage	(157)

ACEIs, angiotensin converting enzyme inhibitors; ARBs, angiotensin receptor blockers; BCL6, B-cell lymphoma 6; CCBs, calcium channel blockers; eNOS, endothelial nitric oxide synthase; LDL, low density lipoprotein; NADPH, nicotinamide adenine dinucleotide phosphate; NO, nitric oxide; ROS, reactive oxygen species.