Excessive Respiratory Modulation of Blood Pressure Triggers Hypertension

Publication date: Available online 16 February 2017
Source:Cell Metabolism
Author(s): Clément Menuet, Sheng Le, Bowen Dempsey, Angela A. Connelly, Jessica L. Kamar, Nikola Jancovski, Jaspreet K. Bassi, Keryn Walters, Annabel E. Simms, Andrew Hammond, Angelina Y. Fong, Ann K. Goodchild, Simon McMullan, Andrew M. Allen
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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Teaser

Menuet et al. establish a causal link between excessive respiratory modulation of blood pressure, acting via brainstem adrenergic neurons, and the development of hypertension in rats. They further show evidence of similar indicators of abnormal respiratory modulation of sympathetic nerve activity (RespSNA) in humans at risk of developing hypertension.


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