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Diabetes alters neuronal nitric oxide release from rat mesenteric arteries. Role of protein kinase C.
Life Sci. 2000; 66(4):337-45.LS

Abstract

The objective of the present study was to assess the influence of diabetes in the neuronal nitric oxide (NO) release elicited by electrical field stimulation (EFS, 200 mA, 0.3 ms, 1-16 Hz, for 30 s, at 1 min interval) in endothelium-denuded mesenteric artery segments from control and streptozotocin-induced diabetic rats, assessing the influence of protein kinase C (PKC) in this release. N(G)-nitro-L-arginine-methyl ester (L-NAME, 10 microM, a NO synthase inhibitor) enhanced EFS-elicited contractions in control, and specially in diabetic rats, whereas they were unaltered by AMT (5 nM, an inducible NO synthase inhibitor) and capsaicin (0.5 microM, a sensory neurone toxin). Calphostin C (0.1 microM, a PKC inhibitor) increased the contraction elicited by EFS in both types of arteries. This increase was further enhanced by calphostin C + L-NAME in diabetic rats. Phorbol 12,13-dibutyrate (PDBu, 1 microM) reduced and unaltered EFS-induced contractions in control and diabetic rats, respectively. The further addition of L-NAME reversed the reduction obtained in control rats, and enhanced the response observed in diabetic rats. These results suggest that the EFS-induced NO release from perivascular nitrergic nerves, that negatively modulates the contraction, which is synthesized by neuronal constitutive NO synthase. The NO synthesis is positively stimulated by PKC. This NO release is increased in diabetes, likely due to an increase in the activity of this enzyme. The sensory nerves of these arteries do not seem to be involved in the contractile response.

Authors+Show Affiliations

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

Pub Type(s)

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

Language

eng

PubMed ID

10665985

Citation

Ferrer, M, et al. "Diabetes Alters Neuronal Nitric Oxide Release From Rat Mesenteric Arteries. Role of Protein Kinase C." Life Sciences, vol. 66, no. 4, 2000, pp. 337-45.
Ferrer M, Marín J, Balfagón G. Diabetes alters neuronal nitric oxide release from rat mesenteric arteries. Role of protein kinase C. Life Sci. 2000;66(4):337-45.
Ferrer, M., Marín, J., & Balfagón, G. (2000). Diabetes alters neuronal nitric oxide release from rat mesenteric arteries. Role of protein kinase C. Life Sciences, 66(4), 337-45.
Ferrer M, Marín J, Balfagón G. Diabetes Alters Neuronal Nitric Oxide Release From Rat Mesenteric Arteries. Role of Protein Kinase C. Life Sci. 2000;66(4):337-45. PubMed PMID: 10665985.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diabetes alters neuronal nitric oxide release from rat mesenteric arteries. Role of protein kinase C. AU - Ferrer,M, AU - Marín,J, AU - Balfagón,G, PY - 2000/2/9/pubmed PY - 2000/3/4/medline PY - 2000/2/9/entrez SP - 337 EP - 45 JF - Life sciences JO - Life Sci VL - 66 IS - 4 N2 - The objective of the present study was to assess the influence of diabetes in the neuronal nitric oxide (NO) release elicited by electrical field stimulation (EFS, 200 mA, 0.3 ms, 1-16 Hz, for 30 s, at 1 min interval) in endothelium-denuded mesenteric artery segments from control and streptozotocin-induced diabetic rats, assessing the influence of protein kinase C (PKC) in this release. N(G)-nitro-L-arginine-methyl ester (L-NAME, 10 microM, a NO synthase inhibitor) enhanced EFS-elicited contractions in control, and specially in diabetic rats, whereas they were unaltered by AMT (5 nM, an inducible NO synthase inhibitor) and capsaicin (0.5 microM, a sensory neurone toxin). Calphostin C (0.1 microM, a PKC inhibitor) increased the contraction elicited by EFS in both types of arteries. This increase was further enhanced by calphostin C + L-NAME in diabetic rats. Phorbol 12,13-dibutyrate (PDBu, 1 microM) reduced and unaltered EFS-induced contractions in control and diabetic rats, respectively. The further addition of L-NAME reversed the reduction obtained in control rats, and enhanced the response observed in diabetic rats. These results suggest that the EFS-induced NO release from perivascular nitrergic nerves, that negatively modulates the contraction, which is synthesized by neuronal constitutive NO synthase. The NO synthesis is positively stimulated by PKC. This NO release is increased in diabetes, likely due to an increase in the activity of this enzyme. The sensory nerves of these arteries do not seem to be involved in the contractile response. SN - 0024-3205 UR - https://www.unboundmedicine.com/medline/citation/10665985/Diabetes_alters_neuronal_nitric_oxide_release_from_rat_mesenteric_arteries__Role_of_protein_kinase_C_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024320599005950 DB - PRIME DP - Unbound Medicine ER -