4.8 Article

Excessive Respiratory Modulation of Blood Pressure Triggers Hypertension

Journal

CELL METABOLISM
Volume 25, Issue 3, Pages 739-748

Publisher

CELL PRESS
DOI: 10.1016/j.cmet.2017.01.019

Keywords

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Funding

  1. National Health and Medical Research Council of Australia (APP) [1029396, 1102477]
  2. Australian Research Council [DP1094301, DP120100920]
  3. McKenzie Research Fellowship from the University of Melbourne
  4. National Health and Medical Research Council of Australia [1102477] Funding Source: NHMRC
  5. Australian Research Council [DP1094301] Funding Source: Australian Research Council

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The etiology of hypertension, the world's biggest killer, remains poorly understood, with treatments targeting the established symptom, not the cause. The development of hypertension involves increased sympathetic nerve activity that, in experimental hypertension, may be driven by excessive respiratory modulation. Using selective viral and cell lesion techniques, we identify adrenergic C1 neurons in the medulla oblongata as critical for respiratory-sympathetic entrainment and the development of experimental hypertension. We also show that a cohort of young, normotensive humans, selected for an exaggerated blood pressure response to exercise and thus increased hypertension risk, has enhanced respiratory-related blood pressure fluctuations. These studies pinpoint a specific neuronal target for ameliorating excessive sympathetic activity during the developmental phase of hypertension and identify a group of pre-hypertensive subjects that would benefit from targeting these cells.

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