ArticleMolecular and cellular biochemistry1996
ATP-sensitive potassium channels are altered in ventricular myocytes from diabetic rats.
Article in Molecular and cellular biochemistry, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- Ischemic preconditioning: Interruption of various disorders.Journal of the Saudi Heart Association · 2017Review
- Mechanisms of sudden cardiac death: oxidants and metabolism.Circulation research · 2015Review
- Hyperoxic preconditioning fails to confer additional protection against ischemia-reperfusion injury in acute diabetic rat heart.EXCLI journal · 2012Article
- The diabetic heart: too sweet for its own good?Cardiology research and practice · 2012Article
- Preconditioning the diabetic human myocardium.Journal of cellular and molecular medicine · 2010Article
- Subcellular mechanisms of adaptation in the diabetic myocardium: Relevance to ischemic preconditioning in the nondiseased heart.Experimental and clinical cardiology · 2010Article
- Cardiac metabolism and arrhythmias.Circulation. Arrhythmia and electrophysiology · 2009Review
- Ischemic tolerance of rat hearts in acute and chronic phases of experimental diabetes.Molecular and cellular biochemistry · 2003Article
- Absence of ischemic preconditioning protection in diabetic sheep hearts: role of sarcolemmal KATP channel dysfunction.Molecular and cellular biochemistry · 2003Article
- Effects of arrhythmogenic lipid metabolites on the L-type calcium current of diabetic vs. non-diabetic rat hearts.Molecular and cellular biochemistry · 2001Article
- Acute diabetes modulates response to ischemia in isolated rat heart.Molecular and cellular biochemistry · 2000Article
- The Influence of Diabetes Mellitus in Myocardial Ischemic Preconditioning.Journal of diabetes researchReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Hypoxia-induced shortening of the action potential duration, attributed to activation of the ATP-sensitive potassium (KATP) channels, occurs to a much greater extent in ventricular cells from diabetic rats. This study examined whether the KATP channels are altered in streptozotocin-diabetic myocardium. In inside-out patches from ventricular myocytes (with symmetrical 140 mM [K+]), inward KATP currents (at potentials negative to the K+ reversal potential) were similar in amplitude in control and diabetic patches (slope conductances: 69 and 74 pS, respectively). However, outward single-channel currents were larger for channels from diabetic heart cells than from control cells (e.g., at +75 mV the diabetic channel currents were 3.7 +/- 0.3 pA vs. 2.7 +/- 0.1 pA for control currents, p < 0.05), due to reduced inward rectification of diabetic channel currents. There was no difference in open and closed times between control and diabetic channels. The IC50 for ATP inhibition of the KATP channel single-channel currents was 11.4 microM for control currents and 4.7 microM for diabetic channel currents. Thus, the major difference found between KATP channels from control and diabetic hearts was the greater outward diabetic single-channel current, which may contribute to the enhanced sensitivity to hypoxia (or ischemia) in diabetic hearts.
Indexed as
Identifiers
8791283What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.