Excessive Respiratory Modulation of Blood Pressure Triggers Hypertension
Autor: | Simon McMullan, Angela A. Connelly, Jessica Kamar, Angelina Y. Fong, Annabel E. Simms, Clément Menuet, Ann K. Goodchild, Jaspreet K. Bassi, Bowen Dempsey, Andrew M. Allen, Keryn Walters, Sheng Le, Nikola Jancovski, Andrew Hammond |
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Rok vydání: | 2017 |
Předmět: |
Aging
medicine.medical_specialty Sympathetic nervous system Sympathetic Nervous System Physiology Blood Pressure 030204 cardiovascular system & hematology Lesion 03 medical and health sciences 0302 clinical medicine Rats Inbred SHR Internal medicine Renin–angiotensin system medicine Animals Molecular Biology Neurons business.industry Respiration Cell Biology Rostral ventrolateral medulla medicine.disease Endocrinology Blood pressure medicine.anatomical_structure Pathophysiology of hypertension Hypertension Synapses Medulla oblongata Carotid body medicine.symptom business 030217 neurology & neurosurgery |
Zdroj: | Cell Metabolism. 25:739-748 |
ISSN: | 1550-4131 |
DOI: | 10.1016/j.cmet.2017.01.019 |
Popis: | 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. |
Databáze: | OpenAIRE |
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