ArticleThe Journal of membrane biology1995
Modulation of the inwardly rectifying K+ channel in isolated human atrial myocytes by alpha 1-adrenergic stimulation.
Article in The Journal of membrane biology, 1995. 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, 32 citations in OpenAlex.
- Autonomic dysregulation and atrial arrhythmias.American journal of physiology. Cell physiology · 2025Review
- Long Non-coding RNA Involved in the Pathophysiology of Atrial Fibrillation.Cardiovascular drugs and therapy · 2025Review
- The Autonomic Coumel Triangle: A New Way to Define the Fascinating Relationship between Atrial Fibrillation and the Autonomic Nervous System.Life (Basel, Switzerland) · 2023Review
- Inhibition of Cardiac Kir Current (IK1) by Protein Kinase C Critically Depends on PKCβ and Kir2.2.PloS one · 2016Article
- Article
- Inhibition of a TREK-like K+ channel current by noradrenaline requires both β1- and β2-adrenoceptors in rat atrial myocytes.Cardiovascular research · 2014Article
- Role of the autonomic nervous system in atrial fibrillation: pathophysiology and therapy.Circulation research · 2014Review
- Cardiac alpha1-adrenergic receptors: novel aspects of expression, signaling mechanisms, physiologic function, and clinical importance.Pharmacological reviews · 2014Review
- Cardiac adrenergic control and atrial fibrillation.Naunyn-Schmiedeberg's archives of pharmacology · 2010Review
- Inhibition of cardiomyocyte automaticity by electrotonic application of inward rectifier current from Kir2.1 expressing cells.Medical & biological engineering & computing · 2006Article
- Modulation of inwardly rectifying potassium channels in cultured bovine pulmonary artery endothelial cells.The Journal of physiology · 1997Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have examined the alpha 1-adrenergic modulation of the inwardly-rectifying K+ channel (IK1) in isolated human atrial myocytes using the patch clamp technique. alpha 1-Adrenergic agonist methoxamine produced action potential prolongation and a depolarization of the resting membrane potential. Under whole-cell voltage-clamp conditions, bath application of methoxamine can inhibit macroscopic IK1. The methoxamine-induced inhibition was reversible and concentration dependent, with the concentration for half-maximal inhibition being 18 microM. The methoxamine-induced inhibition of IK1 was prevented by bath application of alpha 1-adrenergic blocker prazosin. The current was similarly inhibited by phorbol ester (PMA), an activator of protein kinase C (PKC). In contrast, methoxamine failed to inhibit the current in the presence of a specific PKC inhibitor H-9, suggesting that PKC is involved in the methoxamine-induced inhibition of IK1. In single channel recording from cell-attached patches, bath-applied methoxamine could suppress IK1 channels by decreasing the frequency and duration of bursting without affecting unitary amplitude. Direct application of purified PKC to excised inside-out patches inhibited channel activity similar to methoxamine in cell-attached patches. The PKC selective inhibitor, PKC19-36, prevented the PKC-induced inhibition of the channel. We conclude that human atrial IK1 can be inhibited by alpha 1-adrenergic stimulation via PKC-dependent pathways.
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