TY - JOUR
T1 - Intermittent hypoxia
T2 - Cause of or therapy for systemic hypertension?
AU - Serebrovskaya, Tatiana V.
AU - Manukhina, Eugenia B.
AU - Smith, Michael L.
AU - Downey, H. Fred
AU - Mallet, Robert T.
N1 - Funding Information:
This work was supported by grants from the U.S. National Institutes of Health (AT-003598), the Science and Technology Center in Ukraine (4299), and the Russian Foundation for Basic Research (07-04-00650).
PY - 2008/6
Y1 - 2008/6
N2 - During acute episodes of hypoxia, chemoreceptor-mediated sympathetic activity increases heart rate, cardiac output, peripheral resistance and systemic arterial pressure. However, different intermittent hypoxia paradigms produce remarkably divergent effects on systemic arterial pressure in the post- hypoxic steady state. The hypertensive effects of obstructive sleep apnea (OSA) vs. the depressor effects of therapeutic hypoxia exemplify this divergence. OSA, a condition afflicting 15-25% of American men and 5-10% of women, has been implicated in the pathogenesis of systemic hypertension and is a major risk factor for heart disease and stroke. OSA imposes a series of brief, intense episodes of hypoxia and hypercapnia, leading to persistent, maladaptive chemoreflex-mediated activation of the sympathetic nervous system which culminates in hypertension. Conversely, extensive evidence in animals and humans has shown controlled intermittent hypoxia conditioning programs to be safe, efficacious modalities for prevention and treatment of hypertension. This article reviews the pertinent literature in an attempt to reconcile the divergent effects of intermittent hypoxia therapy and obstructive sleep apnea on hypertension. Special emphasis is placed on research conducted in the nations of the former Soviet Union, where intermittent hypoxia conditioning programs are being applied therapeutically to treat hypertension in patients. Also reviewed is evidence regarding mechanisms of the pro- and anti-hyper-tensive effects of intermittent hypoxia.
AB - During acute episodes of hypoxia, chemoreceptor-mediated sympathetic activity increases heart rate, cardiac output, peripheral resistance and systemic arterial pressure. However, different intermittent hypoxia paradigms produce remarkably divergent effects on systemic arterial pressure in the post- hypoxic steady state. The hypertensive effects of obstructive sleep apnea (OSA) vs. the depressor effects of therapeutic hypoxia exemplify this divergence. OSA, a condition afflicting 15-25% of American men and 5-10% of women, has been implicated in the pathogenesis of systemic hypertension and is a major risk factor for heart disease and stroke. OSA imposes a series of brief, intense episodes of hypoxia and hypercapnia, leading to persistent, maladaptive chemoreflex-mediated activation of the sympathetic nervous system which culminates in hypertension. Conversely, extensive evidence in animals and humans has shown controlled intermittent hypoxia conditioning programs to be safe, efficacious modalities for prevention and treatment of hypertension. This article reviews the pertinent literature in an attempt to reconcile the divergent effects of intermittent hypoxia therapy and obstructive sleep apnea on hypertension. Special emphasis is placed on research conducted in the nations of the former Soviet Union, where intermittent hypoxia conditioning programs are being applied therapeutically to treat hypertension in patients. Also reviewed is evidence regarding mechanisms of the pro- and anti-hyper-tensive effects of intermittent hypoxia.
KW - Angiogenesis
KW - Hypertension
KW - Intermittent hypoxia
KW - Nitric oxide
KW - Obstructive sleep apnea
KW - Reactive oxygen species
UR - http://www.scopus.com/inward/record.url?scp=46449128281&partnerID=8YFLogxK
U2 - 10.3181/0710-MR-267
DO - 10.3181/0710-MR-267
M3 - Short survey
C2 - 18408145
AN - SCOPUS:46449128281
SN - 1535-3702
VL - 233
SP - 627
EP - 650
JO - Experimental Biology and Medicine
JF - Experimental Biology and Medicine
IS - 6
ER -