Obligatory Roles of Protein Kinase C and Nitric Oxide in the Regulation of Cerebral Vascular Tone: An Implication of a Pathogenesis of Vasospasm After Subarachnoid Haemorrhage

1998 ◽  
Vol 140 (10) ◽  
pp. 1063-1068 ◽  
Author(s):  
S. Nishizawa ◽  
N. Yokota ◽  
T. Yokoyama ◽  
K. Uemura
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Subarachnoid Haemorrhage ◽  
Vascular Tone ◽  
Kinase C ◽  
Cerebral Vascular

scholarly journals Nitric Oxide and Effects of Cationic Polypeptides in Canine Cerebral Arteries

1997 ◽  
Vol 17 (4) ◽  
pp. 470-480 ◽  
Author(s):  
Hiroyuki Kinoshita ◽  
Zvonimir S. Katusic
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Nitric Oxide Synthase ◽  
Vascular Tone ◽  
Dextran Sulfate ◽  
Cerebral Arteries ◽  
Kinase C ◽  
Basilar Arteries ◽  
Oxide Synthase

Cationic polypeptides are released by activated leukocytes and may play an important role in the regulation of vascular tone. Effects of cationic polypeptides on cerebral vascular tone have not been studied. The present experiments were designed to determine if synthetic cationic polypeptides, poly-L-arginine and poly-L-lysine, affect the function of cerebral arteries. Rings of canine basilar arteries with and without endothelium were suspended for isometric force recording. Poly-L-arginine (10–8–10–7 M) and poly-L-lysine (10–8–10–7 M) caused endothelium-dependent relaxations. A nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (10–4 M), and a nitric oxide scavenger, oxyhemoglobin (3 × 10–6 M), inhibited relaxations in response to cationic polypeptides. Negatively charged molecules, heparin (1 U/ml) and dextran sulfate (10 mg/ml), also inhibited relaxations to poly-L-arginine or poly-L-lysine. Higher concentrations of poly-L-arginine (10–6–10–5 M) and poly-L-lysine (10–6–10–5 M) induced endothelium-independent contractions. A protein kinase C inhibitor, staurosporine (10–8 M), abolished these contractions. Heparin (10 U/ml) and dextran sulfate (100 mg/ml) inhibited the contractile effect of cationic polypeptides but did not affect contractions to phorbol 12,13-dibutyrate. Poly-L-arginine (10–6 M) and poly-L-lysine (10–6 M) abolished endothelium-dependent relaxations in response to bradykinin (10–10–10–6 M) or calcium ionophore A23187 (10–9–10–6 M). Heparin (50 U/ml) and dextran sulfate (200 mg/ml) restored endothelium-dependent relaxations to bradykinin (10–10–10–6 M) in arteries exposed to poly-L-arginine (10–6 M) or poly-L-lysine (10–6 M). These studies demonstrate that in the lower concentration range (10–8–10–7 M), poly-L-arginine and poly-L-lysine induce endothelium-dependent relaxations by production of nitric oxide via charge-dependent activation of endothelial nitric oxide synthase. In the higher concentration range (10–6–10–5 M), cationic polypeptides cause endothelium-independent contractions as well as impairment of endothelium-dependent relaxations in response to bradykinin and A23187. These contractions and inhibition of endothelium-dependent relaxations are also mediated by a charge-dependent mechanism and may involve activation of protein kinase C.

scholarly journals Involvement of adenosine in vascular contractile preconditioning

2001 ◽  
Vol 280 (6) ◽  
pp. H2911-H2919 ◽  
Author(s):  
Nagakatsu Harada ◽  
Sadaichi Sakamoto ◽  
Yasuharu Niwa ◽  
Yutaka Nakaya
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Vascular Tone ◽  
Adenine Nucleotides ◽  
Adrenergic Agonist ◽  
Kinase C ◽  
Tonic Level ◽  
Oxide Synthase ◽  
Mechanical Stretching

Measurements of isometric tensions of rat aortic rings revealed the fact that when aortic rings with intact endothelium were precontracted (preconditioned) for 20 min by the α1-adrenergic agonist phenylephrine (10 μM), the tonic level of subsequent contraction by the same agonist was depressed and/or declined regardless of the presence or absence of endothelium during the second contraction. The removal of endothelium before preconditioning showed no such phenomenon. With the use of specific blockers, involvements of adenosine or of ATP-sensitive K+(KATP) channels during preconditioning or second contraction, respectively, were evaluated. Actions of nitric oxide synthase, cyclooxygenase, P2 ATP purinoceptors, or KATP channels during preconditioning appear not to be involved. Exogenous adenosine (up to 100 μM) without endothelium could mimic the preconditioning; however, contractile preconditioning by phenylephrine, mechanical stretching, or activation of protein kinase C needed to be done. The release of adenosine and adenine nucleotides from aortic rings was augmented by phenylephrine or by mechanical stretching of the rings with intact endothelium. Our results suggest that during vasocontraction, endothelium-derived adenosine acquires an ability to protect vascular tone against subsequent repeated contractions by mediating a delayed, possibly indirect, opening of KATP channels.

Oxidative stress in diabetes-induced endothelial dysfunction involvement of nitric oxide and protein kinase C

2003 ◽  
Vol 35 (6) ◽  
pp. 683-694 ◽  
Author(s):  
Flavia Pricci ◽  
Gaetano Leto ◽  
Lorena Amadio ◽  
Carla Iacobini ◽  
Samantha Cordone ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Endothelial Dysfunction ◽  
Kinase C

Gene‐gene interactions in the protein kinase C/endothelial nitric oxide synthase axis impact the hypotensive effects of propofol

2021 ◽  
Author(s):  
Gustavo H. Oliveira‐Paula ◽  
Daniela A. Pereira ◽  
Lucas C. Pinheiro ◽  
Graziele C. Ferreira ◽  
Waynice N. Paula‐Garcia ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Gene Interactions ◽  
Kinase C ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Mechanism of Hepatic Heme Oxygenase-1 Induction by Isoflurane

2006 ◽  
Vol 104 (1) ◽  
pp. 101-109 ◽  
Author(s):  
Alexander Hoetzel ◽  
Daniel Leitz ◽  
Rene Schmidt ◽  
Eva Tritschler ◽  
Inge Bauer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Phospholipase A2 ◽  
Heme Oxygenase ◽  
Kupffer Cell ◽  
Cell Function ◽  
Heme Oxygenase 1 ◽  
Gadolinium Chloride ◽  
Kinase C

Background The heme oxygenase pathway represents a major cell and organ protective system in the liver. The authors recently showed that isoflurane and sevoflurane up-regulate the inducible isoform heme oxygenase 1 (HO-1). Because the activating cascade remained unclear, it was the aim of this study to identify the underlying mechanism of this effect. Methods Rats were anesthetized with pentobarbital intravenously or with isoflurane per inhalation (2.3 vol%). Kupffer cell function was inhibited by dexamethasone or gadolinium chloride. Nitric oxide synthases were inhibited by either N(omega)-nitro-L-arginine methyl ester or S-methyl thiourea. N-acetyl-cysteine served as an antioxidant, and diethyldithiocarbamate served as an inhibitor of cytochrome P450 2E1. Protein kinase C and phospholipase A2 were inhibited by chelerythrine or quinacrine, respectively. HO-1 was analyzed in liver tissue by Northern blot, Western blot, immunostaining, and enzymatic activity assay. Results In contrast to pentobarbital, isoflurane induced HO-1 after 4-6 h in hepatocytes in the pericentral region of the liver. The induction was prevented in the presence of dexamethasone (P < 0.05) and gadolinium chloride (P < 0.05). Inhibition of nitric oxide synthases or reactive oxygen intermediates did not affect isoflurane-mediated HO-1 up-regulation. In contrast, chelerythrine (P < 0.05) and quinacrine (P < 0.05) resulted in a blockade of HO-1 induction. Conclusion The up-regulation of HO-1 by isoflurane in the liver is restricted to parenchymal cells and depends on Kupffer cell function. The induction is independent of nitric oxide or reactive oxygen species but does involve protein kinase C and phospholipase A2.

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