Cilostazol potentiates the opening of mitochondrial Ca2+-activated K+ channels and reduces infarct size in rabbit hearts

Nishida, Hitoshi; Sato, Toshiaki; Fukasawa, Mika; Miyazaki, Masaru; Nakaya, Haruaki

doi:10.1016/j.yjmcc.2007.07.029

Cited by 1 publication

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Oxytocin is a small peptide hormone and binds to its membrane receptors on the endometrial cells to increase the activity of phospholipase C, yielding diacylglycerol, a PKC activator. Our preliminary data indicated that oxytocin potentiates the opening of mitoK ATP channels in a PKCdependent manner and has an infarct size-limiting effect in rabbit Langendorff-perfused hearts (20).…”

Section: Mitok Atp Channel and Pkcmentioning

confidence: 71%

“…Signaling molecules for all of these receptors are released to some degree during PC ischemia and all stimulate Gi-or Gq-linked receptors and ultimately activate PKC (19). Recently, we have found that oxytocin can afford cardioprotection during I/R through the activation of mitoK ATP channels (20). Oxytocin is a small peptide hormone and binds to its membrane receptors on the endometrial cells to increase the activity of phospholipase C, yielding diacylglycerol, a PKC activator.…”

Section: Mitok Atp Channel and Pkcmentioning

confidence: 99%

See 1 more Smart Citation

New Aspects for the Treatment of Cardiac Diseases Based on the Diversity of Functional Controls on Cardiac Muscles: Mitochondrial Ion Channels and Cardioprotection

et al. 2009

Self Cite

View full text Add to dashboard Cite

Mitochondrial ATP-sensitive K + (mitoK ATP ) and Ca 2+ -activated K + (mitoK Ca ) channels exist in cardiac myocytes, and they play key roles in cardioprotection. We have recently reported that K + influx through mitoK ATP or mitoK Ca channels occurs independently of each other and confers cardioprotection in a similar manner. Activation of mitoK ATP channel is augmented by protein kinase C (PKC), whereas mitoK Ca channel is activated by protein kinase A (PKA). However, phosphatidylinositol 3-kinase (PI3-K) is linked to neither mitoK ATP nor mitoK Ca channels. We have demonstrated that bioactive substances modulate the opening of mitoK ATP channels via a PKC-dependent pathway or opening of mitoK Ca channels via a PKA-dependent pathway and thereby protecting the heart from ischemia/reperfusion injury. Several endogenous substances such as adenosine and bradykinin can reduce infarct size by activation of mitoK ATP channels in a PKC-dependent manner. Adrenomedullin, a potent vasodilator peptide, potentiates the opening of mitoK Ca channels by PKA activation. Treatment with adrenomedullin prior to ischemia results in the reduction of infarct size via a PKA-mediated activation of mitoK Ca channels. Thus, some endogenous substances confer cardioprotection via PKA-or PKC-mediated activation of mitoK ATP or mitoK Ca channels.

show abstract

Section: Mitok Atp Channel and Pkcmentioning

confidence: 71%

Section: Mitok Atp Channel and Pkcmentioning

confidence: 99%