Increased cardiac output contributes to the development of chronic intermittent hypoxia‐induced hypertension

New Findings What is the central question of this study? Chronic intermittent hypoxia (CIH)‐induced hypertension is commonly believed to be a consequence of sympathetic nervous system hyperactivity, but direct recordings of chronic vasoconstriction have never been performed hitherto. We determined w...

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Bibliographic Details
Published in:Experimental physiology 2014-10, Vol.99 (10), p.1312-1324
Main Authors: Lucking, Eric F., O'Halloran, Ken D., Jones, James F. X.
Format: Article
Language:English
Subjects:
Animals
Aorta - physiopathology
Blood Pressure - physiology
Cardiac Output - physiology
Hematocrit
Hindlimb - blood supply
Hypertension - etiology
Hypertension - physiopathology
Hypoxia - complications
Hypoxia - physiopathology
Male
Rats
Rats, Wistar
Sympathetic Nervous System - physiopathology
Tachycardia - etiology
Tachycardia - physiopathology
Vascular Remodeling - physiology
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Summary:New Findings What is the central question of this study? Chronic intermittent hypoxia (CIH)‐induced hypertension is commonly believed to be a consequence of sympathetic nervous system hyperactivity, but direct recordings of chronic vasoconstriction have never been performed hitherto. We determined whether chronic vasoconstriction contributes to the development of hypertension in CIH‐exposed animals. What is the main finding and its importance? We found no evidence of chronic vasoconstriction in CIH‐exposed rats; instead, the development of hypertension was due to an increase in cardiac output. This attempt to increase O2 flow may lead to the initial development of hypertension. Increased in cardiac output has never been previously reported and could be an important parameter to measure in sleep apnoea patients. Chronic intermittent hypoxia (CIH) in animal models has been shown to result in hypertension and elevation of sympathetic nervous system activity. Sympathetically mediated vasoconstriction is believed to be the primary mechanism underpinning CIH‐induced hypertension; however, the potential contribution of the heart is largely overlooked. We sought to determine the contribution of cardiac output (CO) and lumbar sympathetic control of the hindlimb circulation to CIH‐induced hypertension. Male Wistar rats (n = 64) were exposed to 2 weeks of CIH [cycles of 90 s hypoxia (5% O2 nadir) and 210 s normoxia] or normoxia for 8 h day−1. Under urethane anaesthesia, CIH‐treated animals developed hypertension (81.4 ± 2.2 versus 91.6 ± 2.4 mmHg; P 
ISSN:0958-0670
1469-445X
DOI:10.1113/expphysiol.2014.080556