Open AccessMechanisms of intermittent hypoxia induced hypertension
Author(s) -
Bosc Laura V. González,
Resta Thomas,
Walker Benjimen,
Kanagy Nancy L.
Publication year - 2010
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2009.00929.x
Subject(s) - intermittent hypoxia , medicine , hypoxia (environmental) , hypoxemia , disease , pulmonary hypertension , sleep apnea , population , vascular disease , stroke (engine) , cardiology , obstructive sleep apnea , oxygen , mechanical engineering , chemistry , environmental health , organic chemistry , engineering
• Introduction • Mechanisms of IH‐induced systemic hypertension ‐ Contribution of the nervous system ‐ Contribution of circulating and vascular factors ‐ Role of transcription factors in the inflammatory and cardiovascular consequences of IH• NF‐κB • NFAT • HIF‐1 • Intermittent hypoxia induced pulmonary hypertension • ConclusionsExposing rodents to brief episodes of hypoxia mimics the hypoxemia and the cardiovascular and metabolic effects observed in patients with obstructive sleep apnoea (OSA), a condition that affects between 5% and 20% of the population. Apart from daytime sleepiness, OSA is associated with a high incidence of systemic and pulmonary hypertension, peripheral vascular disease, stroke and sudden cardiac death. The development of animal models to study sleep apnoea has provided convincing evidence that recurrent exposure to intermittent hypoxia (IH) has significant vascular and haemodynamic impact that explain much of the cardiovascular morbidity and mortality observed in patients with sleep apnoea. However, the molecular and cellular mechanisms of how IH causes these changes is unclear and under investigation. This review focuses on the most recent findings addressing these mechanisms. It includes a discussion of the contribution of the nervous system, circulating and vascular factors, inflammatory mediators and transcription factors to IH‐induced cardiovascular disease. It also highlights the importance of reactive oxygen species as a primary mediator of the systemic and pulmonary hypertension that develops in response to exposure to IH.