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1 Department of Physiology and Pharmacology, School of Medicine, Loma Linda University, Loma Linda 92350; and 2 Department of Pharmacology, College of Medicine, University of California, Irvine, California 92697
In addition to adrenergic
innervation, cerebral arteries also contain neuronal nitric oxide
synthase (nNOS)-expressing nerves that augment adrenergic nerve
function. We examined the impact of development and chronic
high-altitude hypoxia (3,820 m) on nNOS nerve function in near-term
fetal and adult sheep middle cerebral arteries (MCA). Electrical
stimulation-evoked release of norepinephrine (NE) was measured with
HPLC and electrochemical detection, whereas nitric oxide (NO) release
was measured by chemiluminescence. An inhibitor of NO synthase,
N
-nitro-L-arginine methyl ester
(L-NAME), significantly inhibited stimulation-evoked NE
release in MCA from normoxic fetal and adult sheep with no effect in
MCA from hypoxic animals. Addition of the NO donor
S-nitroso-N-acetyl-DL-penicillamine
fully reversed the effect of L-NAME in MCA from normoxic
animals with no effect in MCA from hypoxic animals. Electrical
stimulation caused a significant increase in NO release in MCA from
normoxic animals, an effect that was blocked by the neurotoxin
tetrodotoxin, whereas there was no increase in NO release in MCA from
hypoxic animals. Relative abundance of nNOS as measured by
Western blot analysis was similar in normoxic fetal and adult MCA.
However, after hypoxic acclimitization, nNOS levels dramatically
declined in both fetal and adult MCA. These data suggest that the
function of nNOS nerves declines during chronic high-altitude hypoxia,
a functional change that may be related to a decline in nNOS protein levels.
high-altitude hypoxemia; cerebrovascular circulation; neuronal nitric oxide synthase nerves; development and sympathetic nerve function; recombinant neuronal nitric oxide synthase; norepinephrine release
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