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Am J Physiol Heart Circ Physiol (September 19, 2002). doi:10.1152/ajpheart.00453.2002
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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

Mechanism of Enhanced Calcium Sensitivity and {alpha} 2-AR Vasoreactivity in Chronic NOS Inhibition Hypertension

Rebecca W Carter1* and Nancy L Kanagy1

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 {alpha}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 {alpha}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 {alpha}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{delta} to the membrane in NR aorta, while PKC{alpha} was translocated to the membrane in LHR aorta. Finally, in ionomycin-permeabilized aorta G06976 eliminated enhanced basal and {alpha}2-AR-stimulated calcium sensitivity in LHR aorta but did not affect NR contraction. Together, these data suggest PKC{alpha} contributes to augmented calcium sensitivity and {alpha}2-AR reactivity following chronic NOS inhibition hypertension.




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