Hydrogen gas reduces chronic intermittent hypoxia-induced hypertension by inhibiting sympathetic nerve activity and increasing vasodilator responses via the antioxidation.
Peng GuanXiao-Meng LinSheng-Chang YangYa-Jing GuoWen-Ya LiYa-Shuo ZhaoFu-Yang YuZhi-Min SunJi-Ren AnEn-Sheng JiPublished in: Journal of cellular biochemistry (2018)
Molecular hydrogen is reported to be used medically to ameliorate various systemic pathological conditions. This study aimed to investigate the effect of hydrogen (H2 ) gas on hypertension induced by intermittent hypoxia in rats. The adult rats were exposed to chronic intermittent hypoxia (CIH) 8 hours/day for 5 weeks and/or H 2 gas 2 hours/day. We found that the systolic and diastolic blood pressure (BP) increased significantly in rats exposed to intermittent hypoxia, both of which were markedly attenuated after H treatment. Furthermore, intermittent hypoxia exposure elevated renal sympathetic nerve activity, consistent with plasma norepinephrine. Additionally, H 2 gas significantly improved CIH-induced abnormal vascular relaxation. Nevertheless, inhalation of H 2 gas alone did not cause such changes. Moreover, H 2 gas-treated rats exposed to CIH showed a significant reduction in 8-hydroxy-2 deoxyguanosine content and increases in superoxide dismutase activity, indicating improved oxidative stress. Taken together, these results indicate that H 2 gas has significant effects on the reduction of BP without any side effects. Mechanistically, inhibition of sympathetic activity and reduction of systemic vascular resistance may participate in this process via the antioxidant activity of H 2 .
Keyphrases
- blood pressure
- room temperature
- high intensity
- oxidative stress
- carbon dioxide
- endothelial cells
- left ventricular
- heart failure
- heart rate
- hypertensive patients
- type diabetes
- drug induced
- single molecule
- diabetic rats
- nitric oxide
- adipose tissue
- hydrogen peroxide
- blood glucose
- metabolic syndrome
- endoplasmic reticulum stress
- replacement therapy
- smoking cessation
- stress induced
- induced apoptosis
- arterial hypertension