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Neurogenic and Sympathoexcitatory Actions of NaCl in Hypertension

  • Hypertension and the Brain (M Banach and A Zanchetti, Section Editors)
  • Published:
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Abstract

Excess dietary salt intake is a major contributing factor to the pathogenesis of salt-sensitive hypertension. Strong evidence suggests that salt-sensitive hypertension is attributed to renal dysfunction, vascular abnormalities, and activation of the sympathetic nervous system. Indeed, sympathetic nerve transections or interruption of neurotransmission in various brain centers lowers arterial blood pressure (ABP) in many salt-sensitive models. The purpose of this article is to discuss recent evidence that supports a role of plasma or cerebrospinal fluid hypernatremia as a key mediator of sympathoexcitation and elevated ABP. Both experimental and clinical studies using time-controlled sampling have documented that a diet high in salt increases plasma and cerebrospinal fluid sodium concentration. To the extent it has been tested, acute and chronic elevations in sodium concentration activates the sympathetic nervous system in animals and humans. A further understanding of how the central nervous system detects changes in plasma or cerebrospinal fluid sodium concentration may lead to new therapeutic treatment strategies in salt-sensitive hypertension.

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Acknowledgments

This work was supported by National Heart, Lung, and Blood Institute Grants R01 HL-090826 and R01 HL-113270 (to Sean D. Stocker), American Heart Association Established Investigator Grant (to Sean D. Stocker), and a Grant-In-Aid (to Kevin D. Monahan).

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Sean D. Stocker, Kevin D. Monahan, and Kirsteen N. Browning declare that they have no conflict 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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Stocker, S.D., Monahan, K.D. & Browning, K.N. Neurogenic and Sympathoexcitatory Actions of NaCl in Hypertension. Curr Hypertens Rep 15, 538–546 (2013). https://doi.org/10.1007/s11906-013-0385-9

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