Neural Control of Blood Pressure in Chronic Intermittent Hypoxia

Sleep apnea (SA) is increasing in prevalence and is commonly comorbid with hypertension. Chronic intermittent hypoxia is used to model the arterial hypoxemia seen in SA, and through this paradigm, the mechanisms that underlie SA-induced hypertension are becoming clear. Cyclic hypoxic exposure during...

Full description

Saved in:
Bibliographic Details
Published in:Current hypertension reports 2016-03, Vol.18 (3), p.19-19, Article 19
Main Authors: Shell, Brent, Faulk, Katelynn, Cunningham, J. Thomas
Format: Article
Language:English
Subjects:
Animals
Blood Pressure
Brain - physiopathology
Cardiology
Chronic Disease
Family Medicine
General Practice
Humans
Hypertension
Hypertension - physiopathology
Hypertension and the Brain (S Stocker
Hypertension and the Brain (S Stocker, Section Editor)
Hypoxia - physiopathology
Internal Medicine
Medicine
Medicine & Public Health
Metabolic Diseases
Nephrology
Primary Care Medicine
Section Editor
Sleep Apnea Syndromes - complications
Topical Collection on Hypertension and the Brain
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Sleep apnea (SA) is increasing in prevalence and is commonly comorbid with hypertension. Chronic intermittent hypoxia is used to model the arterial hypoxemia seen in SA, and through this paradigm, the mechanisms that underlie SA-induced hypertension are becoming clear. Cyclic hypoxic exposure during sleep chronically stimulates the carotid chemoreflexes, inducing sensory long-term facilitation, and drives sympathetic outflow from the hindbrain. The elevated sympathetic tone drives hypertension and renal sympathetic activity to the kidneys resulting in increased plasma renin activity and eventually angiotensin II (Ang II) peripherally. Upon waking, when respiration is normalized, the sympathetic activity does not diminish. This is partially because of adaptations leading to overactivation of the hindbrain regions controlling sympathetic outflow such as the nucleus tractus solitarius (NTS), and rostral ventrolateral medulla (RVLM). The sustained sympathetic activity is also due to enhanced synaptic signaling from the forebrain through the paraventricular nucleus (PVN). During the waking hours, when the chemoreceptors are not exposed to hypoxia, the forebrain circumventricular organs (CVOs) are stimulated by peripherally circulating Ang II from the elevated plasma renin activity. The CVOs and median preoptic nucleus chronically activate the PVN due to the Ang II signaling. All together, this leads to elevated nocturnal mean arterial pressure (MAP) as a response to hypoxemia, as well as inappropriately elevated diurnal MAP in response to maladaptations.
ISSN:1522-6417
1534-3111
DOI:10.1007/s11906-016-0627-8