Aortic vasoreactivity during prolonged hypoxia and hypoxia–reoxygenation in senescent rats

Abstract

To determine the effects of prolonged hypoxia and hypoxia–reoxygenation in senescent blood vessels, isolated aortic rings from 4- and 24-month-old (mo) Wistar rats were submitted to prolonged hypoxia (50 min) or hypoxia/reoxygenation (20 min/30 min) and contractile function recorded. Phenylephrine-induced contraction and sodium nitroprusside- and acetylcholine-induced relaxations were measured after hypoxia or after hypoxia/reoxygenation. In 24 mo group, prolonged hypoxia increased (+83%, P<0.01) and prolonged initial hypoxic contraction, while hypoxic relaxation and delayed contraction were unchanged. Relaxation to acetylcholine was more reduced than in 4 mo group while contraction to phenylephrine and relaxation to sodium nitroprusside were similarly impaired. During reoxygenation, contraction was of same amplitude at both ages and the relaxation to acetylcholine was impaired but to a similar extent in both groups. In conclusion, hypoxic stress induces a greater endothelium-injury in senescent aorta, and increased transient hypoxic contraction, without aggravation of late hypoxic contraction. Aging does not exacerbate the impairment of aortic vasoreactivity after hypoxia–reoxygenation, especially endothelium-dependent relaxation, in sharp contrast to prolonged hypoxia. These age-related changes in vascular sensitivity to oxygen deprivation are different from those observed in coronary arteries, indicating that vasoreactivity during such pathological stress strongly depends on the type of vessel, especially during aging.