ArticleCardiovascular research2008
Angiotensin II and myosin light-chain phosphorylation contribute to the stretch-induced slow force response in human atrial myocardium.
Article in Cardiovascular research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026Review
- Piezo1-mediated autophagy promotes immune-inflammatory responses in ankylosing spondylitis.Cell death & disease · 2026Article
- Stem cell-derived heterocellular atrial engineered cardiac tissue with comparisons to native human atrial myocardium.American journal of physiology. Heart and circulatory physiology · 2025Article
- Preparation of Human Atrial Trabeculae for Ex Vivo Analysis of Human Myocardial Function.Methods in molecular biology (Clifton, N.J.) · 2025Article
- KFrontiers in physiology · 2025Article
- Epac1 increases myosin regulatory light-chain phosphorylation, energetic cost of contraction, and susceptibility to heart failure.PloS one · 2025Article
- Impaired Intracellular Calcium Buffering Contributes to the Arrhythmogenic Substrate in Atrial Myocytes From Patients With Atrial Fibrillation.Circulation · 2024Article
- Left Atrial Myocardium in Arterial Hypertension.Cells · 2022Review
- Contractile Behavior of Right Atrial Myocardium of Healthy Rats and Rats with the Experimental Model of Pulmonary Hypertension.International journal of molecular sciences · 2022Article
- Computationally efficient model of myocardial electromechanics for multiscale simulations.PloS one · 2021Article
- Stretch modulation of cardiac contractility: importance of myocyte calcium during the slow force response.Biophysical reviews · 2020Review
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- Role of myosin light chain phosphatase in cardiac physiology and pathophysiology.Journal of molecular and cellular cardiology · 2016Review
- Old dog, new tricks: novel cardiac targets and stress regulation by protein kinase G.Cardiovascular research · 2016Review
- Insights into length-dependent regulation of cardiac cross-bridge cycling kinetics in human myocardium.Archives of biochemistry and biophysics · 2016Article
- Rho kinase signaling pathways during stretch in primary alveolar epithelia.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Mineralocorticoid receptor activation is crucial in the signalling pathway leading to the Anrep effect.The Journal of physiology · 2011Article
- cAMP- and Ca²(+) /calmodulin-dependent protein kinases mediate inotropic, lusitropic and arrhythmogenic effects of urocortin 2 in mouse ventricular myocytes.British journal of pharmacology · 2011Article
- Effects of GsMTx4 on bacterial mechanosensitive channels in inside-out patches from giant spheroplasts.Biophysical journal · 2010Article
- Calcium sensitivity and the Frank-Starling mechanism of the heart are increased in titin N2B region-deficient mice.Journal of molecular and cellular cardiology · 2010Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
aimsStretch is an important regulator of atrial function. The functional effects of stretch on human atrium, however, are poorly understood. Thus, we characterized the stretch-induced force response in human atrium and evaluated the underlying cellular mechanisms. METHODS AND
resultsIsometric twitch force of human atrial trabeculae (n = 252) was recorded (37 degrees C, 1 Hz stimulation) following stretch from 88 (L88) to 98% (L98) of optimal length. [Na(+)](i) and pH(i) were measured using SBFI and BCECF epifluorescence, respectively. Stretch induced a biphasic force increase: an immediate increase [first-phase, Frank-Starling mechanism (FSM)] to approximately 190% of force at L88 followed by an additional slower increase [5-10 min; slow force response (SFR)] to approximately 120% of the FSM. FSM and SFR were unaffected by gender, age, ejection fraction, and pre-medication with major cardiovascular drugs. There was a positive correlation between the amplitude of the FSM and the SFR. [Na(+)](i) rose by approximately 1 mmol/L and pH(i) remained unchanged during the SFR. Inhibition of Na(+)/H(+)-exchange (3 microM HOE642), Na(+)/Ca(2+)-exchange (5 microM KB-R7943), or stretch-activated channels (0.5 microM GsMtx-4 and 80 microM streptomycin) did not reduce the SFR. Inhibition of angiotensin-II (AngII) receptors (5 microM saralasin and 0.5 microM PD123319) or pre-application of 0.5 microM AngII, however, reduced the SFR by approximately 40-60%. Moreover, stretch increased phosphorylation of myosin light chain 2 (MLC2a) and inhibition of MLC kinase (10 microM ML-7 and 5 microM wortmannin) decreased the SFR by approximately 40-85%.
conclusionStretch elicits a SFR in human atrium. The atrial SFR is mediated by stretch-induced release and autocrine/paracrine actions of AngII and increased myofilament Ca(2+) responsiveness via phosphorylation of MLC2a by MLC kinase.
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Registered trials
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