ArticleThe Journal of physiology1999
ATP counteracts the rundown of gap junctional channels of rat ventricular myocytes by promoting protein phosphorylation.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 48 citations in OpenAlex.
- Cardiac purinergic signalling in health and disease.Purinergic signalling · 2015Review
- Intracellular magnesium-dependent modulation of gap junction channels formed by neuronal connexin36.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Desipramine prevents cardiac gap junction uncoupling.Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
- K ATP channel agonists preserve connexin43 protein in infarcted rats by a protein kinase C-dependent pathway.Journal of cellular and molecular medicine · 2012Article
- Increased myofilament Ca2+-sensitivity and arrhythmia susceptibility.Journal of molecular and cellular cardiology · 2010Review
- Improving cardiac gap junction communication as a new antiarrhythmic mechanism: the action of antiarrhythmic peptides.Naunyn-Schmiedeberg's archives of pharmacology · 2010Review
- RhoA GTPase and F-actin dynamically regulate the permeability of Cx43-made channels in rat cardiac myocytes.The Journal of biological chemistry · 2008Article
- Local effects and mechanisms of antiarrhythmic peptide AAP10 in acute regional myocardial ischemia: electrophysiological and molecular findings.Naunyn-Schmiedeberg's archives of pharmacology · 2008Article
- The connexin turnover, an important modulating factor of the level of cell-to-cell junctional communication: comparison with other integral membrane proteins.The Journal of membrane biology · 2007Review
- Is the junctional uncoupling elicited in rat ventricular myocytes by some dephosphorylation treatments due to changes in the phosphorylation status of Cx43?European biophysics journal : EBJ · 2004Review
- The metabolic inhibitor antimycin A can disrupt cell-to-cell communication by an ATP- and Ca(2+)-independent mechanism.Pflugers Archiv : European journal of physiology · 2003Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The degree of cell-to-cell coupling between ventricular myocytes of neonatal rats appeared well preserved when studied in the perforated version of the patch clamp technique or, in double whole-cell conditions, when ATP was present in the patch pipette solution. In contrast, when ATP was omitted, the amplitude of junctional current rapidly declined (rundown). 2. To examine the mechanism(s) of ATP action, an 'internal perfusion technique' was adapted to dual patch clamp conditions, and reintroduction of ATP partially reversed the rundown of junctional channels. 3. Cell-to-cell communication was not preserved by a non-hydrolysable ATP analogue (5'-adenylimidodiphosphate, AMP-PNP), indicating that the effect most probably did not involve direct interaction of ATP with the channel-forming proteins. 4. An ATP analogue supporting protein phosphorylation but not active transport processes (adenosine 5'-O-(3-thiotriphosphate), ATPgammaS) maintained normal intercellular communication, suggesting that the effect was due to kinase activity rather than to altered intracellular Ca2+. 5. A broad spectrum inhibitor of endogenous serine/threonine protein kinases (H7) reversibly reduced the intercellular coupling. A non-specific exogenous protein phosphatase (alkaline phosphatase) mimicked the effects of ATP deprivation. The non-specific inhibition of endogenous protein phosphatases resulted in the preservation of substantial cell-to-cell communication in ATP-free conditions. 6. The activity of gap junctional channels appears to require both the presence of ATP and protein kinase activity to counteract the tonic activity of endogenous phosphatase(s).
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