The brain melanocortin system, sympathetic control, and obesity hypertension.

@article{daSilva2014TheBM,
  title={The brain melanocortin system, sympathetic control, and obesity hypertension.},
  author={Alexandre A. da Silva and Jussara M. do Carmo and Zhen Wang and John E. Hall},
  journal={Physiology},
  year={2014},
  volume={29 3},
  pages={
          196-202
        }
}
Excess weight gain is the most significant, preventable cause of increased blood pressure (BP) in patients with primary (essential) hypertension and increases the risk for cardiovascular and renal diseases. In this review, we discuss the role of the brain melanocortin system in causing increased sympathetic activity in obesity and other forms of hypertension. In addition, we highlight potential mechanisms by which the brain melanocortin system modulates metabolic and cardiovascular functions. 
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Obesity-Induced Hypertension: Brain Signaling Pathways
TLDR
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.
Melanocortin-4 Receptors and Sympathetic Nervous System Activation in Hypertension
TLDR
MC4R is a potential target for antiobesity therapy, although there are challenges in using MC4R agonists to induce weight loss without evoking increases in SNS activity.
Obesity-induced hypertension: interaction of neurohumoral and renal mechanisms.
TLDR
With prolonged obesity and development of target organ injury, obesity-associated hypertension becomes more difficult to control, often requiring multiple antihypertensive drugs and treatment of other risk factors, including dyslipidemia, insulin resistance and diabetes mellitus, and inflammation.
Leptin, the Autonomic Nervous System, and Hypertension
TLDR
The crosstalk between peripheral signals and activation of CNS pathways (e.g. leptin) in key hypothalamic and brainstem areas that regulate energy balance, SNS activity, and BP represents a potential target for treating obesity and its metabolic and cardiovascular consequences.
Role of the Melanocortin System in the Central Regulation of Cardiovascular Functions
TLDR
The current knowledge of how the melanocortin system influences essential cardiovascular functions, such as blood pressure and heart rate, and its protective role in ischemic events is discussed, with a particular focus on the central regulation of such mechanisms.
Interaction of Neurohumoral and Renal Mechanisms
TLDR
With prolonged obesity and development of target organ injury, especially renal injury, obesity-associated hypertension becomes more difficult to control, often requiring multiple antihypertensive drugs and treatment of other risk factors, including dyslipidemia, insulin resistance and diabetes mellitus, and inflammation.
Should the sympathetic nervous system be a target to improve cardiometabolic risk in obesity?
TLDR
Preliminary evidence is encouraging, but more trials are needed to investigate whether sympathetic inhibition could be used in obesity to reverse or prevent cardiometabolic disease development and the potential benefits of sympathoinhibition on metabolic and cardiovascular functions.
Central role for melanocortin-4 receptors in offspring hypertension arising from maternal obesity
TLDR
It is shown that maternal obesity permanently resets the responsiveness of the central sympathetic nervous system via this pathway, and neonatal leptin exposure is the primary mediator, thereby contributing to offspring hypertension.
Obesity, kidney dysfunction and hypertension: mechanistic links
TLDR
The authors discuss the complex interactions between renal, hormonal and nervous system factors that link excess adiposity with elevated blood pressure and chronic obesity-associated hypertension.
Origin of Aberrant Blood Pressure and Sympathetic Regulation in Diet-Induced Obesity
TLDR
The VMH is the likely origin of leptin-mediated sympathoexcitation and &agr;-MSH hypersensitivity that contribute to obesity-related hypertension.
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