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Dexamethasone decreases neuronal nitric oxide release in mesenteric arteries from hypertensive rats through decreased protein kinase C activation.
Clin Sci (Lond). 2009 Aug 24; 117(8):305-12.CS

Abstract

Neuronal NO plays a functional role in many vascular tissues, including MAs (mesenteric arteries). Glucocorticoids alter NO release from endothelium and the CNS (central nervous system), but no results from peripheral innervation have been reported. In the present study we investigated the effects of dexamethasone on EFS (electrical field stimulation)-induced NO release in MAs from WKY (Wistar-Kyoto) rats and SHRs (spontaneously hypertensive rats) and the role of PKC (protein kinase C) in this response. In endothelium-denuded MAs, L-NAME (NG-nitro-L-arginine methyl ester) increased the contractile response to EFS only in segments from SHRs. EFS-induced contraction was reduced by 1 micromol/l dexamethasone in segments from SHRs, but not WKY rats, and this effect was abolished in the presence of dexamethasone. EFS induced a tetrodotoxin-resistant NO release in WKY rat MAs, which remained unchanged by 1 micromol/l dexamethasone. In SHR MAs, dexamethasone decreased basal and EFS-induced neuronal NO release, and this decrease was prevented by the glucocorticoid receptor antagonist mifepristone. Dexamethasone did not affect nNOS [neuronal NOS (NO synthase)] expression in either strain. In SHR MAs, incubation with calphostin C (a non-selective PKC inhibitor), Gö6983 (a classic PKC delta and zeta inhibitor), LY379196 (a PKCbeta inhibitor) or PKCzeta-PI (PKCzeta pseudosubstrate inhibitor) decreased both basal and EFS-induced neuronal NO release. Additionally, PKC activity was reduced by dexamethasone. The PKC inhibitor-induced reduction in NO release was unaffected by dexamethasone. In conclusion, results obtained in the present study indicate that PKC activity positively modulates the neuronal NO release in MAs from SHRs. They also reveal that by PKC inhibition, through activation of glucocorticoid receptors, dexamethasone reduces neuronal NO release in these arteries.

Authors+Show Affiliations

Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, Arzobispo Morcillo, 4, Madrid 28029, Spain.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19267693

Citation

Aras-López, Rosa, et al. "Dexamethasone Decreases Neuronal Nitric Oxide Release in Mesenteric Arteries From Hypertensive Rats Through Decreased Protein Kinase C Activation." Clinical Science (London, England : 1979), vol. 117, no. 8, 2009, pp. 305-12.
Aras-López R, Xavier FE, Ferrer M, et al. Dexamethasone decreases neuronal nitric oxide release in mesenteric arteries from hypertensive rats through decreased protein kinase C activation. Clin Sci (Lond). 2009;117(8):305-12.
Aras-López, R., Xavier, F. E., Ferrer, M., & Balfagón, G. (2009). Dexamethasone decreases neuronal nitric oxide release in mesenteric arteries from hypertensive rats through decreased protein kinase C activation. Clinical Science (London, England : 1979), 117(8), 305-12. https://doi.org/10.1042/CS20080178
Aras-López R, et al. Dexamethasone Decreases Neuronal Nitric Oxide Release in Mesenteric Arteries From Hypertensive Rats Through Decreased Protein Kinase C Activation. Clin Sci (Lond). 2009 Aug 24;117(8):305-12. PubMed PMID: 19267693.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dexamethasone decreases neuronal nitric oxide release in mesenteric arteries from hypertensive rats through decreased protein kinase C activation. AU - Aras-López,Rosa, AU - Xavier,Fabiano E, AU - Ferrer,Mercedes, AU - Balfagón,Gloria, Y1 - 2009/08/24/ PY - 2009/3/10/entrez PY - 2009/3/10/pubmed PY - 2009/11/5/medline SP - 305 EP - 12 JF - Clinical science (London, England : 1979) JO - Clin Sci (Lond) VL - 117 IS - 8 N2 - Neuronal NO plays a functional role in many vascular tissues, including MAs (mesenteric arteries). Glucocorticoids alter NO release from endothelium and the CNS (central nervous system), but no results from peripheral innervation have been reported. In the present study we investigated the effects of dexamethasone on EFS (electrical field stimulation)-induced NO release in MAs from WKY (Wistar-Kyoto) rats and SHRs (spontaneously hypertensive rats) and the role of PKC (protein kinase C) in this response. In endothelium-denuded MAs, L-NAME (NG-nitro-L-arginine methyl ester) increased the contractile response to EFS only in segments from SHRs. EFS-induced contraction was reduced by 1 micromol/l dexamethasone in segments from SHRs, but not WKY rats, and this effect was abolished in the presence of dexamethasone. EFS induced a tetrodotoxin-resistant NO release in WKY rat MAs, which remained unchanged by 1 micromol/l dexamethasone. In SHR MAs, dexamethasone decreased basal and EFS-induced neuronal NO release, and this decrease was prevented by the glucocorticoid receptor antagonist mifepristone. Dexamethasone did not affect nNOS [neuronal NOS (NO synthase)] expression in either strain. In SHR MAs, incubation with calphostin C (a non-selective PKC inhibitor), Gö6983 (a classic PKC delta and zeta inhibitor), LY379196 (a PKCbeta inhibitor) or PKCzeta-PI (PKCzeta pseudosubstrate inhibitor) decreased both basal and EFS-induced neuronal NO release. Additionally, PKC activity was reduced by dexamethasone. The PKC inhibitor-induced reduction in NO release was unaffected by dexamethasone. In conclusion, results obtained in the present study indicate that PKC activity positively modulates the neuronal NO release in MAs from SHRs. They also reveal that by PKC inhibition, through activation of glucocorticoid receptors, dexamethasone reduces neuronal NO release in these arteries. SN - 1470-8736 UR - https://www.unboundmedicine.com/medline/citation/19267693/Dexamethasone_decreases_neuronal_nitric_oxide_release_in_mesenteric_arteries_from_hypertensive_rats_through_decreased_protein_kinase_C_activation_ L2 - https://portlandpress.com/clinsci/article-lookup/doi/10.1042/CS20080178 DB - PRIME DP - Unbound Medicine ER -