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1 Department of Pharmacology
and Physiology,
To examine
effects of development and chronic high-altitude hypoxia on sympathetic
nerve function in sheep, norepinephrine release was measured in vitro
from middle cerebral and facial arteries. Capsaicin was used to test
the role of capsaicin-sensitive sensory nerves; norepinephrine release
was not altered by capsaicin treatment.
N
-nitro-L-arginine methyl ester
(L-NAME), an inhibitor of NO
synthase, decreased stimulation-evoked norepinephrine release in middle cerebral arteries from normoxic sheep with no effect in hypoxic arteries or facial arteries. Thus NO-releasing nerves augmented norepinephrine release. Furthermore, the function of NO-releasing nerves declined after chronic hypoxia. Despite loss of the augmenting effects of NO, stimulation-evoked fractional norepinephrine release was
unchanged after chronic hypoxia, suggesting that middle cerebral arteries adapt to hypoxia by increasing stimulation-evoked
norepinephrine release. In fetal facial arteries, chronic hypoxia
resulted in a decline in stimulation-evoked norepinephrine release, but
there was an increase in the adult facial artery. In the adult,
adaptation to chronic hypoxia is similar in both cerebral and facial
arteries. However, differential adaptation in fetal adrenergic nerves
may reflect differences in fetal redistribution of blood flow in the face of chronic hypoxia but could also possibly contribute to increased
incidence of fetal morbidity.
nitric oxide synthase; chronic hypoxia; sympathetic nerve function
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