Abstract
BackgroundHypobaric intermittent hypoxia (HIH) produces many favorable effects in the cardiovascular system such as anti-hypertensive effect. In this study, we showed that HIH significantly attenuated a depressor response induced by acute hypoxia.Methodology/Principal FindingsSprague-Dawley rats received HIH in a hypobaric chamber simulating an altitude of 5000 m. The artery blood pressure (ABP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded in anesthetized control rats and rats received HIH. The baseline ABP, HR and RSNA were not different between HIH and control rats. Acute hypoxia-induced decrease in ABP was significantly attenuated in HIH rat compared with control rats. However, acute hypoxia-induced increases in HR and RSNA were greater in HIH rat than in control rats. After removal of bilateral ascending depressor nerves, acute hypoxia-induced depressor and sympathoexcitatory responses were comparable in control and HIH rats. Furthermore, acute hypoxia-induced depressor and sympathoexcitatory responses did not differ between control and HIH groups after blocking ATP-dependent K+ channels by glibenclamide. The baroreflex function evaluated by intravenous injection of phenylephrine and sodium nitroprusside was markedly augmented in HIH rats compared with control rats. The pressor and sympathoexcitatory responses evoked by intravenous injection of cyanide potassium were also significantly greater in HIH rats than in control rats.Conclusions/SignificanceOur findings suggest that HIH suppresses acute hypoxia-induced depressor response through enhancement of baroreflex and chemoreflex function, which involves activation of ATP-dependent K+ channels. This study provides new information and underlying mechanism on the beneficiary effect of HIH on maintaining cardiovascular homeostasis.
Highlights
Prolonged expose to intermittent hypoxia, which mimics obstructive sleep apnea, is associated with an increase in basal arterial blood pressure and sympathetic outflow in animal and human [1,2,3,4,5]
We found that Hypobaric intermittent hypoxia (HIH) attenuated the acute hypoxia-induced depressor response through enhancement of sympathetic outflow and increase in heart rate (HR)
The sympathoexcitatory response is an important component to encounter the depressor response induced by acute hypoxia, which is caused by local vasodilation in response to a reduced blood oxygen concentration [16,17]
Summary
Prolonged expose to intermittent hypoxia, which mimics obstructive sleep apnea, is associated with an increase in basal arterial blood pressure and sympathetic outflow in animal and human [1,2,3,4,5]. HIH produces many favorable effects in the cardiovascular system such as anti-hypertensive effect [9]. In this regard, HIH decreases arterial pressure in hypertension patients and animals with experimental hypertension [10]. HIH reduces sympathetic activity through an enhancement of baroreflex in patients with sleep apnea [12,13]. Hypobaric intermittent hypoxia (HIH) produces many favorable effects in the cardiovascular system such as anti-hypertensive effect. We showed that HIH significantly attenuated a depressor response induced by acute hypoxia
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