Abstract
Obesity greatly increases the risk for cardiovascular, metabolic, and renal diseases and is one of the most significant and preventable causes of increased blood pressure (BP) in patients with essential hypertension. This review highlights recent advances in our understanding of central nervous system (CNS) signaling pathways that contribute to the etiology and pathogenesis of obesity-induced hypertension. We discuss the role of excess adiposity and activation of the brain leptin-melanocortin system in causing increased sympathetic activity in obesity. In addition, we highlight other potential brain mechanisms by which increased weight gain modulates metabolic and cardiovascular functions. Unraveling the CNS mechanisms responsible for increased sympathetic activation and hypertension and how circulating hormones activate brain signaling pathways to control BP offer potentially important therapeutic targets for obesity and hypertension.
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Acknowledgments
We thank Sydney P. Moak, Jackson Browning, and Calvin Torrey for technical assistance with our experimental studies cited in this review.
Sources of Funding
This research was supported by National Heart, Lung and Blood Institute Grant (PO1HL-51971), the National Institute of General Medical Sciences (P20GM104357), and by an American Heart Association Scientist Development Grant to Jussara M. do Carmo.
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Dr. do Carmo reports grants from National Institutes of Health, American Heart Association, and Palatin Technologies. Dr. Hall reports grants from National Institutes of Health and Palatin Technologies. Drs. da Silva, Wang, Fang, Aberdein, and de Lara Rodriguez report no conflicts of interest.
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This article does not contain any studies with human or animal subjects performed by any of the authors.
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This article is part of the Topical Collection on Secondary Hypertension: Nervous System Mechanisms
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do Carmo, J.M., da Silva, A.A., Wang, Z. et al. Obesity-Induced Hypertension: Brain Signaling Pathways. Curr Hypertens Rep 18, 58 (2016). https://doi.org/10.1007/s11906-016-0658-1
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DOI: https://doi.org/10.1007/s11906-016-0658-1