title: Deactivation of carotid body chemoreceptors by hyperoxia decreases blood pressure in hypertensive patients.
abstract: Previous studies have shown that hyperoxia-induced deactivation of carotid body chemoreceptors reduces sympathetic activity in hypertensive patients but it does not affect blood pressure. The maintenance of blood pressure can be explained by the direct, vasoconstrictive effect of hyperoxia, which offsets diminished sympathetic activity. This study compares the effect of acute hyperoxia on hemodynamic parameters between hypertensive and normotensive subjects. Twelve males with hypertension (age 39.4±2.4 years; body mass index 27.4±1.1 kg m(-2)) and 11 normotensive males (age 39.9±2.7 years; body mass index 25.4±0.7 kg m(-2)) received, via non-rebreathing mask ventilation, ambient air, followed by 100% oxygen for 20 min. The stroke volume, heart rate, cardiac output, blood pressure, total peripheral resistance, respiratory rate, baroreceptor control of heart rate and oxygen saturation were recorded continuously. Several 30 s periods were analyzed before, during and after inducing hyperoxia. At baseline, the hypertensive subject's blood pressure was higher and their baroreflex control of heart rate was lower when compared with the normotensive control group. After the first 30 s of hyperoxia, systolic, diastolic and mean blood pressures, as well as the total peripheral resistance, decreased significantly in hypertensives but not in normotensives. After 20 min of 100% oxygen ventilation, systolic and mean blood pressures and total peripheral resistance was increased in hypertensive patients, and the cardiac output and stroke volume had decreased in both groups. The results of this study confirm that deactivation of carotid body chemoreceptors can acutely decrease blood pressure in humans.
authors.affiliation: Department of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, Warsaw, Poland.
authors.forename: Maciej
authors.initials: M
authors.lastname: Sinski
authors.affiliation: Department of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, Warsaw, Poland.
authors.forename: Jacek
authors.initials: J
authors.lastname: Lewandowski
authors.affiliation: Department of Biophysics and Physiology, Medical University of Warsaw, Warsaw, Poland.
authors.forename: Jacek
authors.initials: J
authors.lastname: Przybylski
authors.affiliation: Department of Hygiene and Epidemiology, Faculty of Health Sciences Ludwik Rydygier Collegium Medicum in Bydgoszcz Nicolaus Copernicus University in Torun, Bydgoszcz, Poland.
authors.forename: Paweł
authors.initials: P
authors.lastname: Zalewski
authors.affiliation: Department of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, Warsaw, Poland.
authors.forename: Bartosz
authors.initials: B
authors.lastname: Symonides
authors.affiliation: Department of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, Warsaw, Poland.
authors.forename: Piotr
authors.initials: P
authors.lastname: Abramczyk
authors.affiliation: Department of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, Warsaw, Poland.
authors.forename: Zbigniew
authors.initials: Z
authors.lastname: Gaciong
mesh_terms: D000328:Adult; D017704:Baroreflex / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D002344:Carotid Body / Q000378:metabolism / Q000503:physiopathology*; D002628:Chemoreceptor Cells / Q000378:metabolism*; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D018496:Hyperoxia / Q000378:metabolism / Q000503:physiopathology*; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D008297:Male