ArticleCardiovascular diabetology2012
Increase of ATP-sensitive potassium (K(ATP)) channels in the heart of type-1 diabetic rats.
Article in Cardiovascular diabetology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- O-GlcNAc-modified SNAP29 inhibits autophagy-mediated degradation via the disturbed SNAP29-STX17-VAMP8 complex and exacerbates myocardial injury in type I diabetic rats.International journal of molecular medicine · 2018Article
- Remote ischemic conditioning in ST-segment elevation myocardial infarction - an update.Conditioning medicine · 2018Article
- Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection.Cardiovascular diabetology · 2017Review
- Article
- The application of remote ischemic conditioning in cardiac surgery.F1000Research · 2017Review
- Cardiovascular microRNAs: as modulators and diagnostic biomarkers of diabetic heart disease.Cardiovascular diabetology · 2014Review
- Kir6.2-containing ATP-sensitive K(+) channel is required for cardioprotection of resveratrol in mice.Cardiovascular diabetology · 2014Article
- Protein kinase RNA-like endoplasmic reticulum kinase (PERK) signaling pathway plays a major role in reactive oxygen species (ROS)-mediated endoplasmic reticulum stress-induced apoptosis in diabetic cardiomyopathy.Cardiovascular diabetology · 2013Article
- Role of Kir6.2 subunits of ATP-sensitive potassium channels in endotoxemia-induced cardiac dysfunction.Cardiovascular diabetology · 2013Article
- High-dose fasudil preserves postconditioning against myocardial infarction under hyperglycemia in rats: role of mitochondrial KATP channels.Cardiovascular diabetology · 2012Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAn impairment of cardiovascular function in streptozotocin (STZ)-diabetic rats has been mentioned within 5 days-to-3 months of induction. ATP-sensitive potassium (K(ATP)) channels are expressed on cardiac sarcolemmal membranes. It is highly responsive to metabolic fluctuations and can have effects on cardiac contractility. The present study attempted to clarify the changes of cardiac K(ATP) channels in diabetic disorders.
methodsStreptozotocin-induced diabetic rats and neonatal rat cardiomyocytes treated with a high concentration of glucose (a D-glucose concentration of 30 mM was used and cells were cultured for 24 hr) were used to examine the effect of hyperglycemia on cardiac function and the expression of K(ATP) channels. K(ATP) channels expression was found to be linked to cardiac tonic dysfunction, and we evaluated the expression levels of K(ATP) channels by Western blot and Northern blot analysis.
resultsThe result shows diazoxide produced a marked reduction of heart rate in control group. Furthermore, the methods of Northern blotting and Western blotting were employed to identify the gene expression of K(ATP) channel. Two subunits of cardiac K(ATP) channel (SUR2A and kir 6.2) were purchased as indicators and showed significantly decreased in both diabetic rats and high glucose treated rat cardiac myocytes. Correction of hyperglycemia by insulin or phlorizin restored the gene expression of cardiac K(ATP) in these diabetic rats.
conclusionsBoth mRNA and protein expression of cardiac K(ATP) channels are decreased in diabetic rats induced by STZ for 8 weeks. This phenomenon leads to result in desensitization of some K(ATP) channel drugs.
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