Journal
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
Volume 165, Issue 1, Pages 90-96Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.resp.2008.10.013
Keywords
Blood pressure; Heart rate; Intermittent hypoxia
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Funding
- National Heart Lung and Blood Institute [HL-074072]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL074072] Funding Source: NIH RePORTER
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In rats, acute exposure to hypoxia causes a decrease in mean arterial pressure (MAP) caused by a predominance of hypoxic vasodilation over chemoreflex-induced vasoconstriction. We previously demonstrated that exposure to chronic intermittent hypoxia (CIH) impairs hypoxic vasodilation in isolated resistance arteries; therefore, we hypothesized that the acute systemic hemodynamic responses to hypoxia would be altered by exposure to CIH. To test this hypothesis, rats were exposed to CIH for 14 days. Heart rate (HR) and MAP were monitored by telemetry. On the first day of CIH exposure, acute episodes ofhypoxia caused a decrease in MAP (-9 +/- L 5 mmHg) and an increase in HR (+45 +/- 4 beats/min). On the 14th day of CIH exposure the depressor response was attenuated (-4 +/- 1 mmHg; 44% of the day 1 response) and the tachycardia was enhanced (+68 +/- 2 beats/min; 151% of the day 1 response). The observed time-dependent modulation of the acute hemodynamic responses to hypoxia may reflect important changes in neurocirculatory regulation that contribute to CIH-induced hypertension. (C) 2008 Elsevier B.V. All rights reserved.
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