ArticleThe Journal of physiology1996
Acetylcholine inhibits Ca2+ current by acting exclusively at a site proximal to adenylyl cyclase in frog cardiac myocytes.
Article in The Journal of physiology, 1996. 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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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.
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Who cites it
11 citing papers in PubMed, 29 citations in OpenAlex.
- Regulation of cardiac function by cAMP nanodomains.Bioscience reports · 2023Review
- Adenosine reduces sinoatrial node cell action potential firing rate by uncoupling its membrane and calcium clocks.Frontiers in physiology · 2022Article
- Cardiac cAMP: production, hydrolysis, modulation and detection.Frontiers in pharmacology · 2015Review
- Sinoatrial tissue of crucian carp heart has only negative contractile responses to autonomic agonists.BMC physiology · 2010Article
- Cholinergic receptor signaling modulates spontaneous firing of sinoatrial nodal cells via integrated effects on PKA-dependent Ca(2+) cycling and I(KACh).American journal of physiology. Heart and circulatory physiology · 2009Article
- Muscarinic regulation of cardiac ion channels.British journal of pharmacology · 2003Review
- S100A1: a regulator of myocardial contractility.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Quantitative studies of enzyme-substrate compartmentation, functional coupling and metabolic channelling in muscle cells.Molecular and cellular biochemistry · 1998Article
- Role of the NO-cGMP pathway in the muscarinic regulation of the L-type Ca2+ current in human atrial myocytes.The Journal of physiology · 1998Article
- Longitudinal distribution of Na+ and Ca2+ channels and beta-adrenoceptors on the sarcolemmal membrane of frog cardiomyocytes.The Journal of physiology · 1997Article
- cGMP-stimulated cyclic nucleotide phosphodiesterase regulates the basal calcium current in human atrial myocytes.The Journal of clinical investigation · 1997Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of acetylcholine (ACh) on the L-type Ca2+ current (ICa) stimulated by isoprenaline (Iso) or forskolin (Fsk) were examined in frog ventricular myocytes using the whole-cell patch-clamp technique and a double capillary for extracellular microperfusion. 2. The exposure of one half of the cell to 1 microM Iso produced a half-maximal increase in ICa since a subsequent application of Iso to the other half induced an additional effect of nearly the same amplitude. Similarly, addition of 1 microM ACh to only one half of a cell exposed to Iso on both halves reduced the effect of Iso by only approximately 50%. 3. When 10 microM Iso or 30 microM Fsk were applied to a Ca(2+)-free solution on one half of the cell, ICa was increased in the remote part of the cell where adenylyl cyclase activity was not stimulated. However, addition of ACh (3-10 microM) to the remote part had no effect on ICa, while addition of ACh to the part of the cell exposed to Iso or Fsk strongly antagonized the stimulatory effects of these drugs. 4. Our data demonstrate that ACh regulates ICa by acting at a site proximal to adenylyl cyclase in frog ventricular cells. We conclude that the muscarinic regulation of ICa does not involve any additional cAMP-independent mechanisms occurring downstream from cAMP generation.
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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.