Role of protein kinase C in electrical-stimulation-induced neuronal nitric oxide release in mesenteric arteries from hypertensive rats

2000 ◽  
Vol 99 (4) ◽  
pp. 277 ◽  
Author(s):  
Jesús MARÍN ◽  
Mercedes FERRER ◽  
Gloria BALFAGÓN
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Electrical Stimulation ◽  
Protein Kinase ◽  
Mesenteric Arteries ◽  
Hypertensive Rats ◽  
Nitric Oxide Release ◽  
Kinase C

Diabetes alters neuronal nitric oxide release from rat mesenteric arteries. Role of protein kinase C

Life Sciences ◽  
1999 ◽  
Vol 66 (4) ◽  
pp. 337-345 ◽  
Author(s):  
Mercedes Ferrer ◽  
Jesús Marín ◽  
Gloria Balfagón
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Mesenteric Arteries ◽  
Nitric Oxide Release ◽  
Kinase C

Role of protein kinase C in electrical-stimulation-induced neuronal nitric oxide release in mesenteric arteries from hypertensive rats

2000 ◽  
Vol 99 (4) ◽  
pp. 277-283 ◽  
Author(s):  
Jesús MARÍN ◽  
Mercedes FERRER ◽  
Gloria BALFAGÓN
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
No Synthase ◽  
Mesenteric Arteries ◽  
Protein Synthesis Inhibitor ◽  
Hypertensive Rats ◽  
Wky Rats ◽  
Kinase C ◽  
No Release

This study examines the influence of hypertension on neuronal nitric oxide (NO) release and its modulation by protein kinase C (PKC). For this purpose, mesenteric segments without endothelium were obtained from Wistar–Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs), and neurogenic NO release induced by electrical field stimulation (EFS) was examined in these segments. EFS induced frequency-dependent contractions. The NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and the sensorial neurotoxin capsaicin increased EFS-induced contractions in SHR segments, but did not affect these contractions in segments from WKY rats. In segments from SHRs, the increase in EFS-induced response by capsaicin was further increased by the combination of capsaicin and L-NAME. EFS-induced contractions in SHR arteries were unaltered by the protein synthesis inhibitor cycloheximide or by 2-amine-5,6-dihydro-6-methyl-4H-1,3-tiazine (AMT), an inhibitor of inducible NO synthase, and increased by the guanylate cyclase inhibitor Methylene Blue. In these arteries, capsaicin plus the PKC inhibitor calphostin C increased the contractions elicited by EFS; the addition of L-NAME did not affect this increase. Phorbol 12,13-dibutyrate (PDBu) did not modify the response to EFS in these arteries pretreated with capsaicin, although a combination of PDBu and L-NAME was effective. These results indicate that, in mesenteric arteries, EFS induces the release of NO from perivascular nitrergic nerves and of neuropeptides from sensory nerves, but only in hypertensive rats. The NO released is synthesized by constitutive neuronal NO synthase in a manner that is positively modulated by PKC, an enzyme that seems to be activated in hypertension.

Dexamethasone decreases neuronal nitric oxide release in mesenteric arteries from hypertensive rats through decreased protein kinase C activation

2009 ◽  
Vol 117 (8) ◽  
pp. 305-312 ◽  
Author(s):  
Rosa Aras-López ◽  
Fabiano E. Xavier ◽  
Mercedes Ferrer ◽  
Gloria Balfagón
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Glucocorticoid Receptors ◽  
Electrical Field Stimulation ◽  
Mesenteric Arteries ◽  
Hypertensive Rats ◽  
Pkc Inhibitor ◽  
Kinase C ◽  
No Release ◽  
Wistar Kyoto

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 μmol/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 μmol/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 δ and ζ inhibitor), LY379196 (a PKCβ inhibitor) or PKCζ-PI (PKCζ 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.

The role of nitric oxide, reactive oxygen species, and protein kinase C in oxytocin-induced cardioprotection in ischemic rat heart

Peptides ◽  
2012 ◽  
Vol 37 (2) ◽  
pp. 314-319 ◽  
Author(s):  
Mahdieh Faghihi ◽  
Ali Mohammad Alizadeh ◽  
Vahid Khori ◽  
Mostafa Latifpour ◽  
Saeed Khodayari
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Rat Heart ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Kinase C

scholarly journals Role of protein kinase C in Ca channel blocker-induced renal arteriolar dilation in spontaneously hypertensive rats

2005 ◽  
Vol 54 (2) ◽  
pp. 102-108 ◽  
Author(s):  
Koichi Hayashi ◽  
Shu Wakino ◽  
Yuri Ozawa ◽  
Koichiro Homma ◽  
Takeshi Kanda ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Spontaneously Hypertensive Rats ◽  
Channel Blocker ◽  
Ca Channel ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Kinase C

scholarly journals Induction of nitric oxide release by MRC OX-44 (anti-CD53) through a protein kinase C-dependent pathway in rat macrophages.

1994 ◽  
Vol 179 (4) ◽  
pp. 1119-1126 ◽  
Author(s):  
L Boscá ◽  
P A Lazo
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Membrane Proteins ◽  
Signaling Pathways ◽  
Cell Biology ◽  
Cell Function ◽  
Inositol Phosphates ◽  
Nitric Oxide Release ◽  
Kinase C

Many membrane proteins are implicated in the control of cell function by triggering specific signaling pathways. There is a new family of membrane proteins, defined by its structural motifs, which includes several lymphoid antigens, but lacks a function. To study its biological role, we determined which signaling pathways are affected by the CD53 antigen, a prototypic member of this family, in rat macrophages. Activation of CD53 by cross-linking results in an increase in inositol phosphates and diacylglycerol and in Ca2+ mobilization, which are insensitive to pertussis or cholera toxins. There is a translocation of protein kinase C to the membrane accompanied by nitric oxide (NO) release in macrophages. This effect is the result of the expression of the inducible nitric oxide synthase (iNOS), which is dependent on protein kinase C and protein synthesis. These results have linked a new receptor with a specific pathway of NO induction and thus have opened up a novel aspect of NO regulation in cell biology.

scholarly journals Role of spinal NMDA receptors, protein kinase C and nitric oxide synthase in the hyperalgesia induced by magnesium deficiency in rats

2001 ◽  
Vol 134 (6) ◽  
pp. 1227-1236 ◽  
Author(s):  
Sophie Begon ◽  
Gisèle Pickering ◽  
Alain Eschalier ◽  
André Mazur ◽  
Yves Rayssiguier ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Nitric Oxide Synthase ◽  
Nmda Receptors ◽  
Magnesium Deficiency ◽  
Kinase C ◽  
Oxide Synthase
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