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2-adrenergic stimulation
during NOS inhibition-induced hypertension
Department of Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131
Increased
vascular resistance during systemic nitric oxide synthase (NOS)
inhibition is dependent on adrenergic vasoconstriction. This study
tested the hypothesis that increased vascular sensitivity to adrenergic
agonists contributes to this vasoconstriction. Superior mesenteric
arteries and thoracic aortae from male Sprague-Dawley rats drinking
water containing
N
-nitro-L-arginine
(L-NNA; 14 days, 60 mg · kg
1 · day1)
and control rats were cut into helical strips, and endothelium was
removed for contractile experiments.
L-NNA arteries were more sensitive to UK-14304
(
2-adrenergic agonist) and
norepinephrine (NE), whereas responses to phenylephrine (PE) were not
different [concentration causing 50% maximal response
(EC50),
L-NNA vs. control: UK-14304,
0.071 vs. 0.71 µmol/l; NE, 1.15 vs. 9.95 nmol/l]. Yohimbine, an
2-selective antagonist, caused
a concentration-dependent inhibition of contraction to NE only in
L-NNA arteries
(EC50 = 6.3 vs. 1.6 nmol/l at 1 nmol/l yohimbine), whereas prazosin shifted NE curves similarly in
arteries from both groups. Yohimbine (10 nmol/l) inhibited contractions
to UK-14304 (EC50 = 59 µmol/l
vs. 17 µmol/l) but not contractions to PE, whereas prazosin inhibited both. These data indicate that
L-NNA-induced hypertension leads to increased sensitivity of prazosin-sensitive
2-adrenoceptors, an
upregulation that could cause the increased vasoconstrictor response to
NE in this model of hypertension.
nitric oxide; nitric oxide synthase; 2-adrenoceptors; UK-14304; vascular smooth muscle
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