ArticleThe Journal of clinical investigation1997
Mechanism of hypoxic K loss in rabbit ventricle.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 67 citations in OpenAlex.
- Pharmacologic ROMK Inhibition Protects Against Myocardial Ischemia Reperfusion Injury.International journal of molecular sciences · 2025Article
- The mechanisms of potassium loss in acute myocardial ischemia: New insights from computational simulations.Frontiers in physiology · 2023Article
- Coordinate adaptations of skeletal muscle and kidney to maintain extracellular [KAmerican journal of physiology. Cell physiology · 2020Article
- Cardiac sympathectomy and spinal cord stimulation attenuate reflex-mediated norepinephrine release during ischemia preventing ventricular fibrillation.JCI insight · 2019Article
- Electrophysiology of Hypokalemia and Hyperkalemia.Circulation. Arrhythmia and electrophysiology · 2017Review
- Non-Mammalian Vertebrates: Distinct Models to Assess the Role of Ion Gradients in Energy Expenditure.Frontiers in endocrinology · 2017Review
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Ventricular repolarization markers for predicting malignant arrhythmias in clinical practice.World journal of clinical cases · 2015Review
- Nutrient restriction preserves calcium cycling and mitochondrial function in cardiac myocytes during ischemia and reperfusion.Cell calcium · 2012Article
- Increased myofilament Ca2+-sensitivity and arrhythmia susceptibility.Journal of molecular and cellular cardiology · 2010Review
- Cariporide given during resuscitation promotes return of electrically stable and mechanically competent cardiac activity.Resuscitation · 2010Article
- Cardiac metabolism and arrhythmias.Circulation. Arrhythmia and electrophysiology · 2009Review
- [Coronary artery disease--relevance of total coronary revascularization on the incidence of malignant arrhythmias].Herzschrittmachertherapie & Elektrophysiologie · 2006Review
- Modeling cardiac ischemia.Annals of the New York Academy of Sciences · 2006Review
- Mechanisms of sudden cardiac death.The Journal of clinical investigation · 2005Review
- Intracellular [Na+] and Na+ pump rate in rat and rabbit ventricular myocytes.The Journal of physiology · 2002Article
- Regulation of ion channels in myocardial cells and protection of ischemic myocardium.Heart failure reviews · 2000Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Although a critical factor causing lethal ischemic ventricular arrhythmias, net cellular K loss during myocardial ischemia and hypoxia is poorly understood. We investigated whether selective activation of ATP-sensitive K (KATP) channels causes net cellular K loss by examining the effects of the KATP channel agonist cromakalim on unidirectional K efflux, total tissue K content, and action potential duration (APD) in isolated arterially perfused rabbit interventricular septa. Despite increasing unidirectional K efflux and shortening APD to a comparable degree as hypoxia, cromakalim failed to induce net tissue K loss, ruling out activation of KATP channels as the primary cause of hypoxic K loss. Next, we evaluated a novel hypothesis about the mechanism of hypoxic K loss, namely that net K loss is a passive reflection of intracellular Na gain during hypoxia or ischemia. When the major pathways promoting Na influx were inhibited, net K loss during hypoxia was almost completely eliminated. These findings show that altered Na fluxes are the primary cause of net K loss during hypoxia, and presumably also in ischemia. Given its previously defined role during hypoxia and ischemia in promoting intracellular Ca overload and reperfusion injury, this newly defined role of intracellular Na accumulation as a primary cause of cellular K loss identifies it as a central pathogenetic factor in these settings.
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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.