Obesity-Induced Hypertension: Brain Signaling Pathways.
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.
Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216, USA. jdocarmo@umc.edu.
Jussara M
JM
do Carmo
Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216, USA.|Barão de Mauá University Center, Rua Ramos de Azevedo, 423, Ribeirão Preto, São Paulo, N/A 14026-050, Brazil.
Alexandre A
AA
da Silva
Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216, USA.
Zhen
Z
Wang
Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216, USA.
Taolin
T
Fang
Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216, USA.
Nicola
N
Aberdein
Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216, USA.
Cecilia E P
CE
de Lara Rodriguez
Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Cardiovascular-Renal Research Center, University of Mississippi Medical Center, 2500 North State St., Jackson, MS, 39216, USA.
John E
JE
Hall
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002490:Central Nervous System / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D009765:Obesity / Q000150:complications*; D015398:Signal Transduction; D012891:Sleep Apnea Syndromes / Q000209:etiology
Blood pressure; Leptin; Melanocortins; Metabolism; Sympathetic nervous system