Abstract
Background: Obstructive sleep apnea (OSA) is strongly correlated with an increased risk of systemic hypertension. However, the link between systemic hypertension and nocturnal apneas remains incompletely understood. Animal studies suggest an implication of the endothelin system. The aim of the present study is to determine if endogenous endothelin plays a role in the increase in blood pressure observed during hypoxic episodes in OSA patients, in addition to peripheral chemoreflex and neural sympathetic activation. Methods: We assessed the effects of the nonspecific endothelin antagonist bosentan (500 mg; Tracleer; Actelion; Basel, Switzerland) on ventilation, hemodynamics, and muscle sympathetic nerve activity (MSNA) during normoxia and isocapnic hypoxia using a randomized, crossover, double-blinded, placebocontrolled study design, and in 13 severely untreated sleep apneic patients (age 50 ± 9 years, apnea-hypopnea index 35 ± 21/h). Results: Hypoxia increased blood pressure, MSNA, and minute ventilation as oxygen saturation decreased. Bosentan suppressed completely the increase in SBP during a 5-min hypoxic challenge (143 ± 5 mmHg during hypoxia vs. 133 ± 5 mmHg during normoxia with placebo and 127 ± 3 mmHg during hypoxia vs. 125 ± 3 mmHg during normoxia under bosentan, P = 0.023). DBP as well as the rise in MSNA and ventilation during isocapnic hypoxia did not differ between bosentan and placebo. Conclusion: Endothelin contributes to the rise in SBP in response to acute hypoxia in patients with severely untreated OSA. This was not due to lower chemoreflex activation with bosentan.
| Original language | English |
|---|---|
| Pages (from-to) | 118-124 |
| Number of pages | 7 |
| Journal | Journal of Hypertension |
| Volume | 35 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 1 2017 |
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Keywords
- Endothelin
- Hypertension
- Hypoxia
- Sleep
- Sympathetic nervous system
ASJC Scopus subject areas
- Internal Medicine
- Physiology
- Cardiology and Cardiovascular Medicine
Cite this
Endothelin contributes to the blood pressure rise triggered by hypoxia in severe obstructive sleep apnea. / Janssen, Christophe; Pathak, Atul; Grassi, Guido; Van De Borne, Philippe.
In: Journal of Hypertension, Vol. 35, No. 1, 01.01.2017, p. 118-124.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Endothelin contributes to the blood pressure rise triggered by hypoxia in severe obstructive sleep apnea
AU - Janssen, Christophe
AU - Pathak, Atul
AU - Grassi, Guido
AU - Van De Borne, Philippe
PY - 2017/1/1
Y1 - 2017/1/1
N2 - Background: Obstructive sleep apnea (OSA) is strongly correlated with an increased risk of systemic hypertension. However, the link between systemic hypertension and nocturnal apneas remains incompletely understood. Animal studies suggest an implication of the endothelin system. The aim of the present study is to determine if endogenous endothelin plays a role in the increase in blood pressure observed during hypoxic episodes in OSA patients, in addition to peripheral chemoreflex and neural sympathetic activation. Methods: We assessed the effects of the nonspecific endothelin antagonist bosentan (500 mg; Tracleer; Actelion; Basel, Switzerland) on ventilation, hemodynamics, and muscle sympathetic nerve activity (MSNA) during normoxia and isocapnic hypoxia using a randomized, crossover, double-blinded, placebocontrolled study design, and in 13 severely untreated sleep apneic patients (age 50 ± 9 years, apnea-hypopnea index 35 ± 21/h). Results: Hypoxia increased blood pressure, MSNA, and minute ventilation as oxygen saturation decreased. Bosentan suppressed completely the increase in SBP during a 5-min hypoxic challenge (143 ± 5 mmHg during hypoxia vs. 133 ± 5 mmHg during normoxia with placebo and 127 ± 3 mmHg during hypoxia vs. 125 ± 3 mmHg during normoxia under bosentan, P = 0.023). DBP as well as the rise in MSNA and ventilation during isocapnic hypoxia did not differ between bosentan and placebo. Conclusion: Endothelin contributes to the rise in SBP in response to acute hypoxia in patients with severely untreated OSA. This was not due to lower chemoreflex activation with bosentan.
AB - Background: Obstructive sleep apnea (OSA) is strongly correlated with an increased risk of systemic hypertension. However, the link between systemic hypertension and nocturnal apneas remains incompletely understood. Animal studies suggest an implication of the endothelin system. The aim of the present study is to determine if endogenous endothelin plays a role in the increase in blood pressure observed during hypoxic episodes in OSA patients, in addition to peripheral chemoreflex and neural sympathetic activation. Methods: We assessed the effects of the nonspecific endothelin antagonist bosentan (500 mg; Tracleer; Actelion; Basel, Switzerland) on ventilation, hemodynamics, and muscle sympathetic nerve activity (MSNA) during normoxia and isocapnic hypoxia using a randomized, crossover, double-blinded, placebocontrolled study design, and in 13 severely untreated sleep apneic patients (age 50 ± 9 years, apnea-hypopnea index 35 ± 21/h). Results: Hypoxia increased blood pressure, MSNA, and minute ventilation as oxygen saturation decreased. Bosentan suppressed completely the increase in SBP during a 5-min hypoxic challenge (143 ± 5 mmHg during hypoxia vs. 133 ± 5 mmHg during normoxia with placebo and 127 ± 3 mmHg during hypoxia vs. 125 ± 3 mmHg during normoxia under bosentan, P = 0.023). DBP as well as the rise in MSNA and ventilation during isocapnic hypoxia did not differ between bosentan and placebo. Conclusion: Endothelin contributes to the rise in SBP in response to acute hypoxia in patients with severely untreated OSA. This was not due to lower chemoreflex activation with bosentan.
KW - Endothelin
KW - Hypertension
KW - Hypoxia
KW - Sleep
KW - Sympathetic nervous system
UR - http://www.scopus.com/inward/record.url?scp=85007490283&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85007490283&partnerID=8YFLogxK
U2 - 10.1097/HJH.0000000000001134
DO - 10.1097/HJH.0000000000001134
M3 - Article
VL - 35
SP - 118
EP - 124
JO - Journal of Hypertension
JF - Journal of Hypertension
SN - 0263-6352
IS - 1
ER -