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Hypobaric intermittent hypoxia attenuates hypoxia-induced depressor response.
1Department of Physiology, Hebei Medical University, Shijiazhuang, China.
Plos One
|August 1, 2012
Summary
Hypobaric intermittent hypoxia (HIH) attenuates acute hypoxia's depressor response by enhancing baroreflex and chemoreflex function. This mechanism helps maintain cardiovascular homeostasis, highlighting a beneficial effect of HIH.
Area of Science:
- Cardiovascular Physiology
- Environmental Physiology
- Hypoxia Research
Background:
- Hypobaric intermittent hypoxia (HIH) is known to confer cardiovascular benefits, including an anti-hypertensive effect.
- Previous research indicates HIH can favorably impact cardiovascular function, but its specific interaction with acute hypoxia responses requires elucidation.
Purpose of the Study:
- To investigate the effect of HIH on the depressor response induced by acute hypoxia in rats.
- To elucidate the underlying mechanisms, including the roles of baroreflex, chemoreflex, and ATP-dependent K+ channels.
Main Methods:
- Sprague-Dawley rats were exposed to HIH simulating 5000m altitude.
- Arterial blood pressure (ABP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were recorded.
- Responses to acute hypoxia, baroreflex loading/unloading, and chemoreflex activation were assessed, with and without glibenclamide (ATP-dependent K+ channel blocker).
Main Results:
- HIH significantly attenuated the acute hypoxia-induced decrease in ABP.
- Acute hypoxia caused greater increases in HR and RSNA in HIH rats compared to controls.
- Enhanced baroreflex and chemoreflex function were observed in HIH rats, involving ATP-dependent K+ channels.
Conclusions:
- HIH suppresses acute hypoxia-induced depressor responses via augmented baroreflex and chemoreflex function.
- Activation of ATP-dependent K+ channels is implicated in this HIH-mediated cardiovascular adaptation.
- This study reveals a key mechanism underlying HIH's beneficial role in maintaining cardiovascular homeostasis.
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