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Telmisartan attenuates myocardial apoptosis induced by chronic intermittent hypoxia in rats: modulation of nitric oxide metabolism and inflammatory mediators

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Abstract

Purpose

NO and NO synthase (NOS) are known to play key roles in the development of myocardial apoptosis induced by ischemia/hypoxia. Current evidence suggests that angiotensin II type 1 receptor blockers, such as telmisartan, lower blood pressure and produce beneficial regulatory effects on NO and NOS. Here, we examined the protective role of telmisartan in myocardial apoptosis induced by chronic intermittent hypoxia (CIH).

Methods

Adult male Sprague–Dawley rats were subjected to 8 h of intermittent hypoxia/day, with/without telmisartan for 8 weeks. Myocardial apoptosis, NO and NOS activity, and levels of inflammatory mediators and radical oxygen species were determined.

Results

Treatment with telmisartan preserved endothelial NOS expression and inhibited inducible NOS and excessive NO generation, while reducing oxidation/nitration stress and inflammatory responses. Administration of telmisartan before CIH significantly ameliorated the CIH-induced myocardial apoptosis.

Conclusions

This study show that pre-CIH telmisartan administration ameliorated myocardial injury following CIH by attenuating CIH-induced myocardial apoptosis via regulation of NOS activity and inhibition of excessive NO generation, oxidation/nitration stress, and inflammatory responses.

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Acknowledgments

This study was funded by the National Natural Science Foundation of PR China (grants 81370185 and 81070067).

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Correspondence to Hui-guo Liu.

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Yuan, X., Zhu, D., Guo, Xl. et al. Telmisartan attenuates myocardial apoptosis induced by chronic intermittent hypoxia in rats: modulation of nitric oxide metabolism and inflammatory mediators. Sleep Breath 19, 703–709 (2015). https://doi.org/10.1007/s11325-014-1081-y

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  • DOI: https://doi.org/10.1007/s11325-014-1081-y

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