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2-
adrenoreceptor-stimulated RhoA and Rho kinase in rat aorta
Cell Biology and Physiology Department, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-5218
We demonstrated that arteries
from rats made hypertensive with chronic nitric oxide (NO) synthase
(NOS) inhibition
(N
-nitro-L-arginine in drinking
water, LHR) have enhanced contractile sensitivity to
2-adrenergic receptors (2-AR) agonist
UK-14304 compared with arteries from normotensive rats (NR). NO may
regulate vascular tone in part through suppression of RhoA and Rho
kinase (ROK). We hypothesized that enhanced RhoA and ROK activity
augments 2-AR contraction in LHR aortic rings. Y-27632
eliminated UK-14304 contraction in LHR and NR aortic rings. The order
of increasing sensitivity to Y-27632 was the following:
endothelium-intact NR, LHR, and endothelium-denuded NR. UK-14304
stimulated RhoA translocation to the membrane fraction in LHR and
denuded NR but not in intact NR aorta. Basally, more RhoA was present
in the membrane fraction in denuded NR than in intact NR or LHR aorta.
Relaxation to S-nitroso-N-acetyl-penicillamine and Y-27632 in denuded ionomycin-permeabilized rings was greater in NR
than in LHR. Together these studies indicate 2-AR
contraction depends on ROK activity more in NR than LHR aorta.
Additionally, endogenous NO may regulate RhoA activation, whereas
chronic NOS inhibition appears to cause RhoA desensitization.
2-adrenergic receptors; vascular smooth
muscle
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