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Articles in PresS, published online ahead of print September 19, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00453.2002
Submitted on May 29, 2002
Accepted on September 9, 2002
2-AR Vasoreactivity in Chronic NOS Inhibition Hypertension
1 Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM, USA
* To whom correspondence should be addressed. E-mail: bcarter{at}salud.unm.edu.
PKC augments calcium sensitivity in spontaneously hypertensive rats and contributes to 
2-AR contraction in rabbit saphenous vein. We have previously shown that denuded aortic rings from L-NNA treated hypertensive rats (LHR) contract more to CaCl2 and to the 2-AR agonist, UK14304 than do rings from normotensive rats (NR). We hypothesized that enhanced PKC activity or a change in PKC isoform contributes to augmented calcium sensitivity and enhanced 2-AR contraction in LHR aorta. Current studies demonstrate that non-isoform specific PKC inhibitors reduced UK14304 contraction in both NR and LHR aorta. However, the calcium-dependent PKC inhibitor, Go6976 only attenuated contraction in LHR aorta. Additionally, UK14304 translocated PKC
to the membrane in NR aorta, while PKC was translocated to the membrane in LHR aorta. Finally, in ionomycin-permeabilized aorta G06976 eliminated enhanced basal and 2-AR-stimulated calcium sensitivity in LHR aorta but did not affect NR contraction. Together, these data suggest PKC contributes to augmented calcium sensitivity and 2-AR reactivity following chronic NOS inhibition hypertension.
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