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Am J Physiol Heart Circ Physiol 284: H309-H316, 2003. First published September 19, 2002; doi:10.1152/ajpheart.00453.2002
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Vol. 284, Issue 1, H309-H316, January 2003

Mechanism of enhanced calcium sensitivity and alpha 2-AR vasoreactivity in chronic NOS inhibition hypertension

Rebecca W. Carter and Nancy L. Kanagy

Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131-5218

PKC augments calcium sensitivity in spontaneously hypertensive rats and contributes to alpha 2-adrenergic receptor (AR) contraction in rabbit saphenous vein. We showed previously that denuded aortic rings from Nomega -nitro-L-arginine-treated hypertensive rats (LHR) contract more to CaCl2 and to the alpha 2-AR agonist UK-14304 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 UK-14304 contraction in both NR and LHR aorta. However, the calcium-dependent PKC inhibitor Gö-6976 only attenuated contraction in LHR aorta. Additionally, UK-14304 translocated PKC-delta to the membrane in NR aorta, whereas PKC-alpha was translocated to the membrane in LHR aorta. Finally, in ionomycin-permeabilized aorta Gö-6976 eliminated enhanced basal and augmented alpha 2-AR-stimulated calcium sensitivity in LHR aorta but did not affect NR contraction. Together, these data suggest that PKC-alpha contributes to augmented calcium sensitivity and alpha 2-AR reactivity after chronic nitric oxide synthase inhibition hypertension.

nitric oxide; alpha 2-adrenergic receptors; protein kinase C; vascular smooth muscle; calcium sensitivity


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