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Articles in PresS, published online ahead of print May 30, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01101.2001
Submitted on December 14, 2001
Accepted on May 23, 2002
2-Adrenoreceptor-Stimulated RhoA and Rho Kinase In Rat Aorta
1 Cell Biology and Physiology, University of New Mexico Health Science Center, Albuquerque, NM, USA
* To whom correspondence should be addressed. E-mail: bcarter{at}salud.unm.edu.
We demonstrated that arteries from rats made hypertensive with chronic NOS inhibition (L-NNA in drinking water, LHR) have enhanced contractile sensitivity to 2-AR agonist UK14304 compared to arteries from normotensive rats (NR). NO may regulate vascular tone in part through suppression of RhoA and ROK. We hypothesized that enhanced RhoA and ROK activity augments 2-AR contraction in LHR aortic rings. Y-27632 eliminated UK14304 contraction in LHR and NR aortic rings. The order of increasing sensitivity to Y-27632 was: endothelium-intact NR, LHR, and endothelium-denuded NR. UK14304 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 SNAP 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, while chronic NOS inhibition appears to cause RhoA desensitization.
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