Hydrogen gas reduces chronic intermittent hypoxia-induced hypertension by inhibiting sympathetic nerve activity and increasing vasodilator responses via the antioxidation.

Abstract

Using a rat model of chronic intermittent hypoxia (CIH) achieved by 8 hours/day exposure over 5 weeks, the effects of H2 gas inhalation (2 hours/day) on cardiovascular parameters were examined. CIH elevated both systolic and diastolic blood pressure, increased renal sympathetic nerve activity, and raised plasma norepinephrine levels. Co-administration of H2 gas markedly reduced these blood pressure elevations and restored abnormal vascular relaxation responses. Oxidative stress markers showed improvement: 8-hydroxy-2-deoxyguanosine content declined while superoxide dismutase activity increased in H2-treated CIH rats. H2 inhalation alone produced no significant cardiovascular changes. The findings suggest that antioxidant activity of H2 underlies suppression of sympathetic nerve activity and reduction of systemic vascular resistance, collectively contributing to blood pressure normalization in CIH-exposed animals.

Mechanism

H2 exerts antioxidant effects—evidenced by increased superoxide dismutase activity and decreased 8-hydroxy-2-deoxyguanosine—which suppress renal sympathetic nerve activity and reduce systemic vascular resistance, thereby attenuating CIH-induced blood pressure elevation.