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Received for publication July 3, 2003.
Revised August 1, 2003.
Accepted for publication September 30, 2003.
These studies examined adrenergic reactivity of
mesenteric arteries and veins from DOCA-salt hypertensive
and SHAM control mice. We measured constrictions in
unpressurized arteries and veins by monitoring vessel
diameter using computer-assisted video microscopy in
vitro. Veins were more sensitive than arteries to the
constricting effects of norepinephrine (NE) and
phenylephrine (PE) but the
2
agonists clonidine and UK 14,304 did not constrict
arteries or veins. Reactivity was not altered in arteries
or veins from DOCA-salt mice. We next investigated the
mechanism of increased venous reactivity to NE and PE by
studying desensitization to maximum concentrations of NE
and PE. SHAM arteries desensitized to NE and PE more than
DOCA-salt arteries while DOCA-salt and SHAM veins
maintained 80% of the initial NE and PE constriction. To
determine if the increased reactivity and resistance to
desensitization in veins was due to a greater
-
adrenoceptor reserve, vessels were incubated with the
alkylating agent phenoxybenzamine (PBZ; 0.3, 3, 10, 30
nM). The NE-elicited initial constriction was reduced by
PBZ (3, 10, 30 nM) in SHAM but only by PBZ (30 nM) in
DOCA-salt veins. All doses of PBZ blocked NE responses in
SHAM and DOCA-salt arteries. These data suggest that
mesenteric veins express more
1
-adrenoceptors than arteries accounting for greater
reactivity and resistance to desensitization compared to
arteries.
Key words:
DOCA-salt hypertension, alpha adrenergic receptors, alpha adrenoceptor reserve, alpha-1 adrenoceptors, mesenteric vasculature, vascular reactivity
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