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The Sympathetic Nervous System in Obesity Hypertension

  • Adrenal and Nervous System Mechanisms (S Oparil, Section Editor)
  • Published:
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Abstract

Abundant evidence supports a role of the sympathetic nervous system in the pathogenesis of obesity-related hypertension. However, the nature and temporal progression of mechanisms underlying this sympathetically mediated hypertension are incompletely understood. Recent technological advances allowing direct recordings of renal sympathetic nerve activity (RSNA) in conscious animals, together with direct suppression of RSNA by renal denervation and reflex-mediated global sympathetic inhibition in experimental animals and human subjects have been especially valuable in elucidating these mechanisms. These studies strongly support the concept that increased RSNA is the critical mechanism by which increased central sympathetic outflow initiates and maintains reductions in renal excretory function, causing obesity hypertension. Potential determinants of renal sympathoexcitation and the differential mechanisms mediating the effects of renal-specific versus reflex-mediated, global sympathetic inhibition on renal hemodynamics and cardiac autonomic function are discussed. These differential mechanisms may impact the efficacy of current device-based approaches for hypertension therapy.

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Acknowledgments

The authors’ studies cited in this report were funded by National Heart, Lung, and Blood Institute Grant HL-51971.

Conflict of Interest

Thomas E. Lohmeier has received consulting fees from CVRx and research support from National Institutes of Health.

Radu Iliescu declares that he has no conflict of interest.

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Lohmeier, T.E., Iliescu, R. The Sympathetic Nervous System in Obesity Hypertension. Curr Hypertens Rep 15, 409–416 (2013). https://doi.org/10.1007/s11906-013-0356-1

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