Long-term exposure to ambient fine particulate pollution (PM2.5) has been associated with cardiovascular diseases. Hypertension, a major risk factor for cardiovascular diseases, has also been hypothesized to be linked to PM2.5. However, epidemiological evidence has been mixed. We examined long-term association between ambient PM2.5 and hypertension and blood pressure. We interviewed 12,665 participants aged 50 years and older and measured their blood pressures. Annual average PM2.5 concentrations were estimated for each community using satellite data. We applied two-level logistic regression models to examine the associations, and estimated hypertension burden attributable to ambient PM2.5. For each 10 μg/m3 increase in ambient PM2.5, the adjusted odds ratio of hypertension was 1.14 (95% confidence interval, 1.07, 1.22). Stratified analyses found that overweight and obesity could enhance the association, and consumption of fruit was associated with lower risk. We further estimated that 11.75% (95% confidence interval: 5.82%, 18.53%) of the hypertension cases (corresponding to 914, 95% confidence interval: 453, 1442 cases) could be attributable to ambient PM2.5 in the study population. Findings suggest that long-term exposure to ambient PM2.5 might be an important risk factor of hypertension, and is responsible for significant hypertension burden in adults in China. A higher consumption of fruit may mitigate, while overweight and obesity could enhance this effect.

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Excessive release of high mobility group box-1 (HMGB1) protein from ischemic cardiomyocytes activates inflammatory cascades and enhances myocardial injury after reperfusion. Here we report evidence that electroacupuncture of mice at Neiguan acupoints can inhibit the up-regulation of cardiac HMGB1 following myocardial ischemia and attenuate the associated inflammatory responses and myocardial injury during reperfusion. These benefits of electroacupuncture were partially reversed by administering recombinant HMGB1 to the mice, and further potentiated by administering anti-HMGB1 antibody. Electroacupuncture-induced inhibition of HMGB1 release was markedly reduced by unilateral vagotomy or administration of nicotinic receptor antagonist, but not by chemical sympathectomy. The cholinesterase inhibitor neostigmine mimicked the effects of electroacupuncture on HMGB1 release and myocardial ischemia reperfusion injury. Culture experiments with isolated neonatal cardiomyocytes showed that acetylcholine, but not noradrenaline, inhibited hypoxia-induced release of HMGB1 via a α7nAchR-dependent pathway. These results suggest that electroacupuncture acts via the vagal nerve and its nicotinic receptor-mediated signaling to inhibit HMGB1 release from ischemic cardiomyocytes. This helps attenuate pro-inflammatory responses and myocardial injury during reperfusion.