ArticleActa pharmacologica Sinica2009
Modulation of K(ATP) currents in rat ventricular myocytes by hypoxia and a redox reaction.
Article in Acta pharmacologica Sinica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Modulation of Redox-Sensitive Cardiac Ion Channels.Antioxidants (Basel, Switzerland) · 2025Review
- Redox Regulation of KAntioxidants & redox signaling · 2024Review
- Glutathione Upregulates the Expression of KBioMed research international · 2023Article
- Nutritional ketosis as an intervention to relieve astrogliosis: Possible therapeutic applications in the treatment of neurodegenerative and neuroprogressive disorders.European psychiatry : the journal of the Association of European Psychiatrists · 2020Review
- Age-dependent electrocardiographic changes in Pgc-1β deficient murine hearts.Clinical and experimental pharmacology & physiology · 2018Article
- Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics.American journal of physiology. Heart and circulatory physiology · 2016Article
- βIV-Spectrin and CaMKII facilitate Kir6.2 regulation in pancreatic beta cells.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Redox control of cardiac excitability.Antioxidants & redox signaling · 2013Review
- Cardiac specific ATP-sensitive K+ channel (KATP) overexpression results in embryonic lethality.Journal of molecular and cellular cardiology · 2012Article
- CaMKII in the cardiovascular system: sensing redox states.Physiological reviews · 2011Review
- Cardiac calmodulin kinase: a potential target for drug design.Current medicinal chemistry · 2011Review
- Adenosine analogue-oligo-arginine conjugates (ARCs) serve as high-affinity inhibitors and fluorescence probes of type I cGMP-dependent protein kinase (PKGIalpha).Biochimica et biophysica acta · 2010Article
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3 authors.
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Abstract
aimThe present study investigated the possible regulatory mechanisms of redox agents and hypoxia on the K(ATP) current (I(KATP)) in acutely isolated rat ventricular myocytes.
methodsSingle-channel and whole-cell patch-clamp techniques were used to record the K(ATP) current (I(KATP)) in acutely isolated rat ventricular myocytes.
resultsOxidized glutathione (GSSG, 1 mmol/L) increased the I(KATP), while reduced glutathione (GSH, 1 mmol/L) could reverse the increased I(KATP) during normoxia. To further corroborate the effect of the redox agent on the K(ATP) channel, we employed the redox couple DTT (1 mmol/L)/H2O2 (0.3, 0.6, and 1 mmol/L) and repeated the previous processes, which produced results similar to the previous redox couple GSH/GSSG during normoxia. H2O2 increased the I(KATP) in a concentration dependent manner, which was reversed by DTT (1 mmol/L). In addition, our results have shown that 15 min of hypoxia increased the I(KATP), while GSH (1 mmol/L) could reverse the increased I(KATP). Furthermore, in order to study the signaling pathways of the I(KATP) augmented by hypoxia and the redox agent, we applied a protein kinase C(PKC) inhibitor bisindolylmaleimide VI (BIM), a protein kinase G(PKG) inhibitor KT5823, a protein kinase A (PKA) inhibitor H-89, and Ca2+/calmodulin-dependent protein kinase II (CaMKII) inhibitors KN-62 and KN-93. The results indicated that BIM, KT5823, KN-62, and KN-93, but not H-89, inhibited the I(KATP) augmented by hypoxia and GSSG; in addition, these results suggest that the effects of both GSSG and hypoxia on K(ATP) channels involve the activation of the PKC, PKG, and CaMK II pathways, but not the PKA pathway.
conclusionThe present study provides electrophysiological evidence that hypoxia and the oxidizing reaction are closely related to the modulation of I(KATP).
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