Abstract
The role of sympathetic nerve activity in hypertension is currently receiving increased attention, because catheter-based renal denervation was recently shown to reduce blood pressure safely in patients with treatment-resistant hypertension. The central nervous system, which regulates sympathetic nerve activity and blood pressure, is pivotal. Central sympathoexcitation has been shown to be deeply involved in the pathogenesis of salt-sensitive hypertension, although its precise mechanisms have not yet been fully elucidated due to their complexity. Recently, a role for brain oxidative stress in sympathoexcitation has been suggested in some hypertensive animal models. We have demonstrated that increased brain oxidative stress may elevate arterial pressure through central sympathoexcitation in salt-sensitive hypertension. Several factors other than oxidative stress have also been shown to play important roles in central sympathetic activation. In the future, strategies may be developed to elicit a sympathetic inhibition by modulating these factors to prevent and manage salt-sensitive hypertension.
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Acknowledgments
This work was supported by grants from the Japan Heart Foundation Research Grant, the Salt Science Research Foundation (No. 1321), the Japan Foundation for Applied Enzymology, and the Japan Vascular Disease Research Foundation.
Conflict of Interest
Megumi Fujita declares that she has no conflict of interest.
Toshiro Fujita has received research support from Takeda, Daiichi-Sankyo, MSD, Boehringer Ingelheim, Mitsubishi Tanabe, Mochida, Omron, Fukuda-Denshi, Kyowa-Kirin, Toray, Astellas, and Chugai and consulting fees and honoraria from Takeda, Novartis, Boehringer Ingelheim, and Astellas.
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Fujita, M., Fujita, T. The Role of CNS in Salt-sensitive Hypertension. Curr Hypertens Rep 15, 390–394 (2013). https://doi.org/10.1007/s11906-013-0358-z
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DOI: https://doi.org/10.1007/s11906-013-0358-z