ArticleInternational journal of cell biology2011
ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume-Overloaded Rats.
Article in International journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Association of Valvular Disease Progression Using Echocardiographic Findings in a Large U.S. Cohort.Echocardiography (Mount Kisco, N.Y.) · 2026Article
- Isosteviol Sensitizes sarcKATP Channels towards Pinacidil and Potentiates Mitochondrial Uncoupling of Diazoxide in Guinea Pig Ventricular Myocytes.Oxidative medicine and cellular longevity · 2016Article
- Effects of IGF-1 on I(K) and I(K1) Channels via PI3K/Akt Signaling in Neonatal Cardiac Myocytes.International journal of cell biology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
ATP-sensitive potassium channels (K(ATP)) protect the myocardium from hypertrophy induced by pressure-overloading. In this study, we determined the effects of these channels in volume-overloading. We compared the effects of a K(ATP) agonist and a K(ATP) antagonist on sarcolemmal transmembrane current density (pA/pF) clamped at 20 mV increments of membrane potential from -80 to +40 mV in ventricular cardiac myocytes. The basal outward potassium pA/pF in myocytes of volume-overloaded animals was significantly smaller than that in the myocytes of sham-operated controls. Treatment of the control myocytes with the K(ATP) agonist cromakalim increased pA/pF significantly. This increase was blocked by the K(ATP) antagonist glibenclamide. Treatment of the hypertrophied myocytes from volume-overloaded animals with cromakalim and in the presence and absence of glibenclamide did not change pA/pF significantly. These findings suggest that eccentrically hypertrophied cardiac myocytes from volume-overloading may be unresponsive to specific activation/inactivation of K(ATP) and that dysfunctional K(ATP) may fail to protect the myocardium from left ventricular hypertrophy associated with volume-overloading.
Identifiers
What OpenQuestion holds
Registered trials
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