14 nights of intermittent hypoxia elevate daytime blood pressure and sympathetic activity in healthy humans.
Obstructive sleep apnoea syndrome (OSAS) causes nocturnal chronic intermittent hypoxia (IH) that contributes to excess cardiovascular morbidity. To explore the consequences of IH, we used our recently developed model of nocturnal IH in healthy humans to characterise the profile of this blood pressure increase, to determine if it is sustained and to explore potential physiological mechanisms. We performed 24-h ambulatory monitoring of blood pressure in 12 healthy subjects before and after 2 weeks of IH exposure. We also assessed systemic haemodynamics, muscle sympathetic nerve activity (MSNA), ischaemic calf blood flow responses and baroreflex gain. We obtained blood samples for inflammatory markers before, during and after exposure. IH significantly increased daytime ambulatory blood pressure after a single night of exposure (3 mmHg for mean and diastolic) and further increased daytime pressures after 2 weeks of exposure (8 mmHg systolic and 5 mmHg diastolic). Mean ± sd MSNA increased across the exposure (17.2 ± 5.1 versus 21.7 ± 7.3 bursts·min⁻¹; p < 0.01) and baroreflex control of sympathetic outflow declined from -965.3 ± 375.1 to -598.4 ± 162.6 AIU·min⁻¹ ·mmHg⁻¹ (p < 0.01). There were no evident changes in either vascular reactivity or systemic inflammatory markers. These data are the first to show that the arterial pressure rise is sustained throughout the waking hours beyond the acute phase immediately after exposure. Moreover, they may suggest that sympathoactivation induced by IH likely contributes to blood pressure elevation and may derive from reduced baroreflex inhibition. These mechanisms may reflect those underlying the blood pressure elevation associated with OSAS.
Sleep Laboratory and EFCR, Dept of Rehabilitation and Physiology, University Hospital, Grenoble, France. rtamisier@chu-grenoble.fr
R
R
Tamisier
J L
JL
Pépin
J
J
Rémy
J P
JP
Baguet
J A
JA
Taylor
J W
JW
Weiss
P
P
Lévy
D052242:Adiponectin / Q000097:blood; D000328:Adult; D001794:Blood Pressure; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000096:biosynthesis; D018946:Chemokine CCL5 / Q000097:blood; D005260:Female; D006801:Humans; D006973:Hypertension / Q000209:etiology; D000860:Hypoxia / Q000503:physiopathology*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D017472:Receptors, Interleukin-1 / Q000096:biosynthesis; D012891:Sleep Apnea Syndromes / Q000150:complications / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D052242:Adiponectin; D018946:Chemokine CCL5; D016209:Interleukin-8; D020738:Leptin; D017472:Receptors, Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein