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2-adrenoceptors are not
present in proximal arterioles of rat intestine
Department of Physiology, West Virginia University School of Medicine, Morgantown, West Virginia 26506-9229
The purpose of
this study was to evaluate two potential stimuli for nitric oxide (NO)
release in rat intestinal arterioles during sympathetic nerve
activation. To determine whether these vessels contain endothelial
2-adrenoceptors linked to the
L-arginine-NO pathway,
intravital microscopy was used to study the response of first-order
arterioles (1As, 20-40 µm ID) to direct application of
1) the selective
2-agonist BHT-933 and
2) norepinephrine (NE) or
sympathetic nerve stimulation before and after
1- or
2-receptor blockade. The effect
of sympathetic nerve stimulation on 1A wall shear rate (WSR) was also
determined to evaluate the possibility of hemodynamic shear stress as a
stimulus for NO release. BHT-933 had no effect on 1A diameter, whereas
NE produced dose-dependent constrictions of 5 ± 3 to 15 ± 3 µm, which were usually abolished by the
1-antagonist prazosin but
unaffected by the
2-antagonist idazoxan. Sympathetic nerve stimulation at 3, 8, and 16 Hz induced constrictions of 4 ± 1, 8 ± 2, and 17 ± 4 µm,
respectively, and these constrictions were also usually abolished by
prazosin but unaffected by idazoxan. Resting WSR averaged 1,997 ± 163 s
1 and decreased to
1,587 ± 209, 1,087 ± 195, and 537 ± 99 s
1 during 3-, 8-, and 16-Hz
nerve stimulation. These results suggest that
2-adrenoceptor-dependent
pathways do not influence either resting tone or sympathetic
constriction of proximal arterioles in the intestinal submucosa and
that luminal shear stress in these vessels significantly decreases with
sympathetic constriction. It therefore appears unlikely that either
2-receptor activation or
changes in hemodynamic shear serve as stimuli for arteriolar NO release
during periods of increased sympathetic nerve activity.
microcirculation; adrenergic receptors; endothelium-derived relaxing factor; nitric oxide; sympathetic nerves
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