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K ATP channel agonists preserve connexin43 protein in infarcted rats by a protein kinase C-dependent pathway.

Lee TM, Lin CC, Lien HY, Chen CC - J. Cell. Mol. Med. (2012)

Bottom Line: Myocardial connexin43 level was significantly decreased in vehicle-treated infarcted rats compared with sham.The beneficial effects of K(ATP) channel agonists were blocked by either glibenclamide or 5-hydroxydecanoate.The specific PKC(ε) antagonist, myristoylated PKC(ε) V1-2 peptide, did not have additional beneficial effects on connexin43 phosphorylation compared with rats treated with nicorandil alone.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Cardiology Section, Taipei Medical University and Chi-Mei Medical Center, Tainan, Taiwan. tsungm.lee@msa.hinet.net

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Inducibility quotient of ventricular arrhythmias by programmed electrical stimulation four weeks after MI. The number of animals in each group is indicated in parentheses. *P < 0.05 compared with vehicle-, glibenclamide (Glib)-, nicorandil (Nic) + Glib- and pinacidil (Pin) + Glib-treated groups. ††P < 0.01 compared with infarcted groups.
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fig07: Inducibility quotient of ventricular arrhythmias by programmed electrical stimulation four weeks after MI. The number of animals in each group is indicated in parentheses. *P < 0.05 compared with vehicle-, glibenclamide (Glib)-, nicorandil (Nic) + Glib- and pinacidil (Pin) + Glib-treated groups. ††P < 0.01 compared with infarcted groups.

Mentions: To further elucidate the physiological effect of enhanced Cx43 level, ventricular pacing was performed. The arrhythmia score in the sham-operated rats was very low (0.08 ± 0.29; Fig. 7). Either nicorandil or pinacidil significantly decreased the inducibility of ventricular tachyarrhythmias compared with the vehicle. The beneficial effects of nicorandil and pinacidil on arrhythmic score were abolished by administering glibenclamide.


K ATP channel agonists preserve connexin43 protein in infarcted rats by a protein kinase C-dependent pathway.

Lee TM, Lin CC, Lien HY, Chen CC - J. Cell. Mol. Med. (2012)

Inducibility quotient of ventricular arrhythmias by programmed electrical stimulation four weeks after MI. The number of animals in each group is indicated in parentheses. *P < 0.05 compared with vehicle-, glibenclamide (Glib)-, nicorandil (Nic) + Glib- and pinacidil (Pin) + Glib-treated groups. ††P < 0.01 compared with infarcted groups.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3822848&req=5

fig07: Inducibility quotient of ventricular arrhythmias by programmed electrical stimulation four weeks after MI. The number of animals in each group is indicated in parentheses. *P < 0.05 compared with vehicle-, glibenclamide (Glib)-, nicorandil (Nic) + Glib- and pinacidil (Pin) + Glib-treated groups. ††P < 0.01 compared with infarcted groups.
Mentions: To further elucidate the physiological effect of enhanced Cx43 level, ventricular pacing was performed. The arrhythmia score in the sham-operated rats was very low (0.08 ± 0.29; Fig. 7). Either nicorandil or pinacidil significantly decreased the inducibility of ventricular tachyarrhythmias compared with the vehicle. The beneficial effects of nicorandil and pinacidil on arrhythmic score were abolished by administering glibenclamide.

Bottom Line: Myocardial connexin43 level was significantly decreased in vehicle-treated infarcted rats compared with sham.The beneficial effects of K(ATP) channel agonists were blocked by either glibenclamide or 5-hydroxydecanoate.The specific PKC(ε) antagonist, myristoylated PKC(ε) V1-2 peptide, did not have additional beneficial effects on connexin43 phosphorylation compared with rats treated with nicorandil alone.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Cardiology Section, Taipei Medical University and Chi-Mei Medical Center, Tainan, Taiwan. tsungm.lee@msa.hinet.net

Show MeSH
Related in: MedlinePlus