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1 Departments of Medicine and Respiratory Disease and 2 Department of Physiology/Biophysics, University of Louisville, Louisville, Kentucky 40292; and 3 The Max Delbruck Center for Molecular Medicine, Humboldt University, 13092 Berlin, Germany
Recurrent
episodic hypoxia (EH) is a feature of sleep apnea that may be
responsible for some chronic cardiovascular sequelae such as systemic
hypertension. Chronic EH (8 h/day for 35 days) causes elevation of
diurnal resting (unstimulated) mean arterial blood pressure (MAP) in
the rat. We used in vivo video microscopy to examine arteriolar
reactivity in the cremaster muscle of male Sprague-Dawley rats
subjected to 35 days of EH. Cremaster muscles of EH (n = 6) and control (n = 6) rats were exposed to varying doses of norepinephrine (NE) (10
10 to 105
M), ACh (109 to 105 M), and endothelin-1
(1012 to 108 M). In a separate experiment,
EH (n = 5) and control (n = 6) rats
were given one dose of a nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl
ester (L-NAME; 105 M). We also examined
endothelial NOS mRNA from the kidneys of EH-stimulated and control
(unstimulated) rats. Telemetry-monitored EH rats showed a 16-mmHg
increase in MAP over 35 days, whereas control rats showed no change.
The response to NE and endothelin-1 were similar for EH and control
rats. ACh vasodilatation of arterioles in EH rats was significantly
attenuated compared with that of controls. The degree of
vasoconstriction in response to blockade of the nitric oxide system by
L-NAME was significantly less (83% of baseline diameter
with L-NAME) for arterioles of EH rats compared with that
for controls (61% of baseline diameter), implying lower basal resting
nitric oxide release in the EH rats. Whole kidney mRNA endothelial NOS
levels were not different between groups. These data support the
hypothesis that chronic elevation of blood pressure associated with EH
involves increased peripheral resistance from decreased basal release
or production of nitric oxide after 35 days of EH.
systemic hypertension; sleep apnea; vasoconstriction; endothelial microvasculature; endothelial nitric oxide synthase mRNA; vasodilation; vascular tone
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