Inhibition by protein kinase C of the 86Rb+ efflux and vasorelaxation induced by P1075, a KATP channel opener, in rat isolated aorta

1997 ◽  
Vol 356 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Claudia Linde ◽  
Cornelia Löffler ◽  
U. Quast
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Katp Channel ◽  
Kinase C ◽  
Channel Opener ◽  
Isolated Aorta ◽  
Katp Channel Opener

Interaction between thiol-modifying agents and P1075, a KATP channel opener, in rat isolated aorta

1997 ◽  
Vol 356 (4) ◽  
pp. 467-474 ◽  
Author(s):  
Claudia Linde ◽  
Cornelia Löffler ◽  
Christina Kessler ◽  
U. Quast
Keyword(s):  
Katp Channel ◽  
Channel Opener ◽  
Isolated Aorta ◽  
Katp Channel Opener

Remifentanil Preconditioning Confers Cardioprotection via  Cardiac κ- and δ-Opioid Receptors

2005 ◽  
Vol 102 (2) ◽  
pp. 371-378 ◽  
Author(s):  
Ye Zhang ◽  
Michael G. Irwin ◽  
Tak Ming Wong ◽  
Mai Chen ◽  
Chun-Mei Cao
Keyword(s):  
At Risk ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Katp Channel ◽  
Area At Risk ◽  
Mitochondrial Katp Channel ◽  
Ringer’S Solution ◽  
Kinase C

Background Remifentanil preconditioning (RPC) reduces the infarct size in anesthetized rat hearts, and this effect seems to be mediated by all three types of opioid receptors (ORs). Because there is evidence of only kappa- and delta- but not mu-ORs in the rat heart, the authors investigated whether RPC confers cardioprotection via cardiac kappa- and delta-OR as well as via extracardiac mu-OR agonist activity. The authors also investigated the involvement of signaling mechanisms, namely protein kinase C and mitochondrial adenosine triphosphate-sensitive potassium (KATP) channels. Methods The hearts of male Sprague-Dawley rats weighing 190-210 g were removed, mounted on a Langendorff apparatus, and perfused retrogradely at 100 cm H2O with Krebs-Ringer's solution. All hearts were subjected to 30 min of ischemia and 2 h of reperfusion. The study consisted of three series of experiments on the effect of ischemic preconditioning or RPC (10, 50, and 100 ng/ml remifentanil) after blockade of OR subtypes (delta-OR antagonist naltrindol, kappa-OR antagonist nor-binaltorphimine, and mu-OR antagonist CTOP). The involvement of protein kinase C or the KATP channel in the cardioprotection of RPC was also investigated using specific blockers in each group. RPC was produced by three cycles of 5-min perfusion of remifentanil in Krebs-Ringer's solution interspersed with a 5-min reperfusion with Krebs solution only. Infarct size, as a percentage of the area at risk, was determined by 2,3,5-triphenyltetrazolium staining. Results Infarct size as a percentage of the area at risk was significantly reduced after RPC from 51.9 +/- 5.0% (control, n = 8) to 36.2 +/- 10.0% (100 ng/ml RPC, n = 8, P < 0.01). This effect was stopped by pretreatment with naltrindol (52.3 +/- 5.2%) and nor-binaltorphimine (43.5 +/- 6.0%) but not CTOP (37.1 +/- 6.0%). Chelerythrine and GF109203X, both protein kinase C inhibitors, abolished the effects of RPC or ischemic preconditioning on infarct size as a percentage of area at risk. 5-Hydroxydecanoate (a selective mitochondrial KATP channel blocker) also abolished the cardioprotection of RPC and IPC, but HMR-1098 (a selective inhibitor of the sarcolemmal KATP channel) did not. Conclusion Cardiac delta- and kappa- but not mu-ORs mediate the cardioprotection produced by RPC. Both protein kinase C and the mitochondrial KATP channel were involved in this effect.

scholarly journals KATP channel agonists preserve connexin43 protein in infarcted rats by a protein kinase C-dependent pathway

2012 ◽  
Vol 16 (4) ◽  
pp. 776-788 ◽  
Author(s):  
Tsung-Ming Lee ◽  
Chih-Chan Lin ◽  
Hsiao-Yin Lien ◽  
Chien-Chang Chen
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Katp Channel ◽  
Kinase C ◽  
Dependent Pathway

scholarly journals Protein kinase C-dependent activation of KATP channel enhances adenosine-induced cardioprotection

1998 ◽  
Vol 336 (2) ◽  
pp. 337-343 ◽  
Author(s):  
Bruce T. LIANG
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Katp Channel ◽  
Receptor Agonist ◽  
Cell Model ◽  
Protective Action ◽  
Channel Activation ◽  
Kinase C ◽  
Adenosine A1 ◽  
Stimulation Of

Prior activation of protein kinase C (PKC) can precondition the cardiac cell against injury during subsequent ischaemia. By using cultured chick ventricular cell model for simulated ischaemia and preconditioning, the present study investigated the biochemical mechanism underlying the PKC-mediated preconditioning. A 5 min exposure to PMA enhanced the ability of pinacidil to mediate cardioprotection during a subsequent 90 min period of ischaemia, which is consistent with a sustained activation of the KATP channel initiated by PKC. The brief prior exposure to PMA was also associated with an enhanced ability of the adenosine A1 or A3 receptor agonist 2-chloro-N6-cyclopentyladenosine or N6-(3-iodobenzyl)adenosine-5´-N-methyluronamide to elicit a cardioprotective response during the subsequent ischaemia. In myocytes pretreated with PMA, the cardioprotection mediated by receptor agonist was blocked by the concomitant presence of KATP-channel antagonists glibenclamide or 5-hydroxydecanoic acid during the ischaemia. Thus the KATP channel acts downstream of the adenosine A1 and A3 receptors in mediating the protective effect due to prior PMA exposure. KATP channel activation is responsible for the adenosine receptor-mediated effect. PMA treatment had no effect on other A1 or A3 receptor-mediated effects such as the inhibition of adenylate cyclase, ruling out a direct stimulation of the receptor or G-protein by PMA. The present results indicate that prior stimulation of PKC causes a sustained KATP channel activation, which in turn renders the myocyte more responsive to the protective action of adenosine A1 and A3 receptor agonists during the subsequent ischaemia.

Opening of mitochondrial KATP channel occurs downstream of PKC-ε activation in the mechanism of preconditioning

2002 ◽  
Vol 283 (1) ◽  
pp. H440-H447 ◽  
Author(s):  
Yoshito Ohnuma ◽  
Tetsuji Miura ◽  
Takayuki Miki ◽  
Masaya Tanno ◽  
Atsushi Kuno ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Left Ventricle ◽  
Infarct Size ◽  
Katp Channel ◽  
The Other ◽  
Particulate Fraction ◽  
K Channel ◽  
Mitochondrial Katp Channel ◽  
Kinase C

We examined whether the mitochondrial ATP-sensitive K channel (KATP) is an effector downstream of protein kinase C-ε (PKC-ε) in the mechanism of preconditioning (PC) in isolated rabbit hearts. PC with two cycles of 5-min ischemia/5-min reperfusion before 30-min global ischemia reduced infarction from 50.3 ± 6.8% of the left ventricle to 20.3 ± 3.7%. PC significantly increased PKC-ε protein in the particulate fraction from 51 ± 4% of the total to 60 ± 4%, whereas no translocation was observed for PKC-δ and PKC-α. In mitochondria separated from the other particulate fractions, PC increased the PKC-ε level by 50%. Infusion of 5-hydroxydecanoate (5-HD), a mitochondrial KATP blocker, after PC abolished the cardioprotection of PC, whereas PKC-ε translocation by PC was not interfered with 5-HD. Diazoxide, a mitochondrial KATP opener, infused 10 min before ischemia limited infarct size to 5.2 ± 1.4%, but this agent neither translocated PKC-ε by itself nor accelerated PKC-ε translocation after ischemia. Together with the results of earlier studies showing mitochondrial KATP opening by PKC, the present results suggest that mitochondrial KATP-mediated cardioprotection occurs subsequent to PKC-ε activation by PC.

Involvement of Protein Kinase C and Na+/K+-ATPase in the Contractile Response Induced by Myricetin in Rat Isolated Aorta

Planta Medica ◽  
2002 ◽  
Vol 68 (2) ◽  
pp. 133-137 ◽  
Author(s):  
Rosario Jiménez ◽  
Antonio Zarzuelo ◽  
Milagros Galisteo ◽  
Juan Duarte
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Contractile Response ◽  
Kinase C ◽  
Isolated Aorta
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