RGD Reference Report - Mechanism of enhanced calcium sensitivity and alpha 2-AR vasoreactivity in chronic NOS inhibition hypertension. - Rat Genome Database

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

Authors: Carter, RW  Kanagy, NL 
Citation: Carter RW and Kanagy NL, Am J Physiol Heart Circ Physiol. 2003 Jan;284(1):H309-16. Epub 2002 Sep 19.
RGD ID: 1642531
Pubmed: PMID:12388232   (View Abstract at PubMed)
DOI: DOI:10.1152/ajpheart.00453.2002   (Journal Full-text)

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 N(omega)-nitro-l-arginine-treated hypertensive rats (LHR) contract more to CaCl(2) 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 Go-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 Go-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.

Objects referenced in this article
Gene Prkcd protein kinase C, delta Rattus norvegicus

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