ArticleThe Journal of physiology2004
Inositol-1,4,5-trisphosphate-dependent Ca(2+) signalling in cat atrial excitation-contraction coupling and arrhythmias.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.
- Calcium and arrhythmogenesis.Physiological reviews · 2007Pooled it
- Modeling the spatiotemporal properties of crosstalk between RyR-mediated and IPFrontiers in cell and developmental biology · 2026Article
- Article
- Mechanisms of stretch-induced electro-anatomical remodeling and atrial arrhythmogenesis.Journal of molecular and cellular cardiology · 2024Review
- Increased Risk for Atrial Alternans in Rabbit Heart Failure: The Role of CaBiomolecules · 2023Article
- Timing mechanisms to control heart rhythm and initiate arrhythmias: roles for intracellular organelles, signalling pathways and subsarcolemmal CaPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Icariin protects cerebral neural cells from ischemia‑reperfusion injury in anExperimental and therapeutic medicine · 2023Article
- GBiomedicines · 2023Article
- Intestinal enteroendocrine cells rely on ryanodine and IPThe Journal of physiology · 2023Article
- The 'Reverse FDUF' Mechanism of Atrial Excitation-Contraction Coupling Sustains Calcium Alternans-A Hypothesis.Biomolecules · 2022Article
- TRPC channels blockade abolishes endotoxemic cardiac dysfunction by hampering intracellular inflammation and CaNature communications · 2022Article
- Inositol 1,4,5-trisphosphate receptors in cardiomyocyte physiology and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Anti-inflammatory effects of endothelin receptor blockade in left atrial tissue of spontaneously hypertensive rats.International journal of cardiology. Heart & vasculature · 2022Article
- Inositol 1,4,5-trisphosphate receptor - reactive oxygen signaling domain regulates excitation-contraction coupling in atrial myocytes.Journal of molecular and cellular cardiology · 2022Article
- Inhibition of CaPflugers Archiv : European journal of physiology · 2021Article
- Modulations of Cardiac Functions and Pathogenesis by Reactive Oxygen Species and Natural Antioxidants.Antioxidants (Basel, Switzerland) · 2021Review
- TRIC-A regulates intracellular CaPflugers Archiv : European journal of physiology · 2021Review
- Excitation-contraction coupling and calcium release in atrial muscle.Pflugers Archiv : European journal of physiology · 2021Review
- Increases in [IP3]i aggravates diastolic [Ca2+] and contractile dysfunction in Chagas' human cardiomyocytes.PLoS neglected tropical diseases · 2020Article
- Calcium Signaling in Cardiomyocyte Function.Cold Spring Harbor perspectives in biology · 2020Review
29 more citing papers are in PubMed but not listed here.
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2 authors at 1 institution in 1 country.
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Abstract
Inositol-1,4,5-trisphosphate (IP(3))-dependent Ca(2+) release represents the major Ca(2+) mobilizing pathway responsible for diverse functions in non-excitable cells. In the heart, however, its role is largely unknown or controversial. In intact cat atrial myocytes, endothelin (ET-1) increased basal [Ca(2+)](i) levels, enhanced action potential-evoked [Ca(2+)](i) transients, caused [Ca(2+)](i) transients with alternating amplitudes (Ca(2+) alternans), and facilitated spontaneous Ca(2+) release from the sarcoplasmic reticulum (SR) in the form of Ca(2+) sparks and arrhythmogenic Ca(2+) waves. These effects were prevented by the IP(3) receptor (IP(3)R) blocker aminoethoxydiphenyl borate (2-APB), suggesting the involvement of IP(3)-dependent SR Ca(2+) release. In saponin-permeabilized myocytes IP(3) and the more potent IP(3)R agonist adenophostin increased basal [Ca(2+)](i) and the frequency of spontaneous Ca(2+) sparks. In the presence of tetracaine to eliminate Ca(2+) release from ryanodine receptor (RyR) SR Ca(2+) release channels, IP(3) and adenophostin triggered unique elementary, non-propagating IP(3)R-dependent Ca(2+) release events with amplitudes and kinetics that were distinctly different from classical RyR-dependent Ca(2+) sparks. The effects of IP(3) and adenophostin were prevented by heparin and 2-APB. The data suggest that IP(3)-dependent Ca(2+) release increases [Ca(2+)](i) in the vicinity of RyRs and thus facilitates Ca(2+)-induced Ca(2+) release during excitation-contraction coupling. It is concluded that in the adult mammalian atrium IP(3)-dependent Ca(2+) release enhances atrial Ca(2+) signalling and exerts a positive inotropic effect. In addition, by facilitating Ca(2+) release, IP(3) may also be an important component in the development of Ca(2+)-mediated atrial arrhythmias.
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