ArticleThe Journal of physiology2004
Activation of Na+-H+ exchange and stretch-activated channels underlies the slow inotropic response to stretch in myocytes and muscle from the rat heart.
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 35 papers.
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Who cites it
35 citing papers in PubMed, 95 citations in OpenAlex.
- Cardiac myosin-binding protein-C acts as a tunable load sensor to regulate afterload dependence of ventricular function.American journal of physiology. Heart and circulatory physiology · 2025Article
- Stretch regulation of β2-Adrenoceptor signalling in cardiomyocytes requires caveolae.Cardiovascular research · 2025Article
- The Anrep effect in septic shock: a mechanism of cardiac adaptation.British journal of anaesthesia · 2025Article
- The Heart Is a Smart Pump: Mechanotransduction Mechanisms of the Frank-Starling Law and the Anrep Effect.Annual review of physiology · 2025Review
- Modeling cardiomyocyte mechanics and autoregulation of contractility by mechano-chemo-transduction feedback.iScience · 2022Article
- The role of activation of two different sGC binding sites by NO-dependent and NO-independent mechanisms in the regulation of SACs in rat ventricular cardiomyocytes.Physiological reports · 2022Article
- Piezo buffers mechanical stress via modulation of intracellular CaFrontiers in physiology · 2022Article
- Review
- CaMKII activity contributes to homeometric autoregulation of the heart: A novel mechanism for the Anrep effect.The Journal of physiology · 2020Article
- Mechano-electric and mechano-chemo-transduction in cardiomyocytes.The Journal of physiology · 2020Review
- Stretch modulation of cardiac contractility: importance of myocyte calcium during the slow force response.Biophysical reviews · 2020Review
- Insights From Computational Modeling Into the Contribution of Mechano-Calcium Feedback on the Cardiac End-Systolic Force-Length Relationship.Frontiers in physiology · 2020Article
- Disruption of Transverse-Tubules Eliminates the Slow Force Response to Stretch in Isolated Rat Trabeculae.Frontiers in physiology · 2020Article
- The lack of slow force response in failing rat myocardium: role of stretch-induced modulation of Ca-TnC kinetics.The journal of physiological sciences : JPS · 2019Article
- Mechano-chemo-transduction in cardiac myocytes.The Journal of physiology · 2017Review
- Cardiac Mechano-Gated Ion Channels and Arrhythmias.Circulation research · 2016Review
- Systems approach to the study of stretch and arrhythmias in right ventricular failure induced in rats by monocrotaline.Progress in biophysics and molecular biology · 2014Article
- Glucagon-like peptide-1 (7-36) but not (9-36) augments cardiac output during myocardial ischemia via a Frank-Starling mechanism.Basic research in cardiology · 2014Article
- Inhibition of iPLA2 β and of stretch-activated channels by doxorubicin alters dystrophic muscle function.British journal of pharmacology · 2013Article
- The autocrine/paracrine loop after myocardial stretch: mineralocorticoid receptor activation.Current cardiology reviews · 2013Review
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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
We present the first direct comparison of the major candidates proposed to underlie the slow phase of the force increase seen following myocardial stretch: (i) the Na(+)-H(+) exchanger (NHE) (ii) nitric oxide (NO) and the ryanodine receptor (RyR) and (iii) the stretch-activated channel (SAC) in both single myocytes and multicellular muscle preparations from the rat heart. Ventricular myocytes were stretched by approximately 7% using carbon fibres. Papillary muscles were stretched from 88 to 98% of the length at which maximum tension is generated (L(max)). Inhibition of NHE with HOE 642 (5 microm) significantly reduced (P < 0.05) the magnitude of the slow force response in both muscle and myocytes. Neither inhibition of phosphatidylinositol-3-OH kinase (PtdIns-3-OH kinase) with LY294002 (10 microm) nor NO synthase with L-NAME (1 mm) reduced the slow force response in muscle or myocytes (P > 0.05), and the slow response was still present in the single myocyte when the sarcoplasmic reticulum was rigorously inhibited with 1 microm ryanodine and 1 microm thapsigargin. We saw a significant reduction (P < 0.05) in the slow force response in the presence of the SAC blocker streptomycin in both muscle (80 microm) and myocytes (40 microm). In fura 2-loaded myocytes, HOE 642 and streptomycin, but not L-NAME, ablated the stretch-induced increase in [Ca(2+)](i) transient amplitude. Our data suggest that in the rat, under our experimental conditions, there are two mechanisms that underlie the slow inotropic response to stretch: activation of NHE; and of activation of SACs. Both these mechanisms are intrinsic to the myocyte.
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