ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Inhibition of the late sodium current slows t-tubule disruption during the progression of hypertensive heart disease in the rat.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Dietary Branched-Chain Amino Acids Modify Postinfarct Cardiac Remodeling and Function in the Murine Heart.Journal of the American Heart Association · 2025Article
- Dietary Branched Chain Amino Acids Modify Post-Infarct Cardiac Remodeling and Function in the Murine Heart.bioRxiv : the preprint server for biology · 2024Article
- Effects of maternal hypothyroidism on postnatal cardiomyocyte proliferation and cardiac disease responses of the progeny.American journal of physiology. Heart and circulatory physiology · 2023Article
- Article
- The Many Faces of Arterial Hypertension in Hypertrophic Cardiomyopathy and Its Phenocopies: Bystander, Consequence, Modifier.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2021Article
- Role of t-tubule remodeling on mechanisms of abnormal calcium release during heart failure development in canine ventricle.American journal of physiology. Heart and circulatory physiology · 2021Article
- Phosphatidylinositol-4,5-Bisphosphate Binding to Amphiphysin-II Modulates T-Tubule Remodeling: Implications for Heart Failure.Frontiers in physiology · 2021Article
- Dapagliflozin Mediates Plin5/PPARα Signaling Axis to Attenuate Cardiac Hypertrophy.Frontiers in pharmacology · 2021Article
- Changes in cellular CaThe Journal of physiology · 2020Article
- T-tubule remodeling and increased heterogeneity of calcium release during the progression to heart failure in intact rat ventricle.Physiological reports · 2017Article
- Ranolazine Prevents Phenotype Development in a Mouse Model of Hypertrophic Cardiomyopathy.Circulation. Heart failure · 2017Article
- Regional distribution of T-tubule density in left and right atria in dogs.Heart rhythm · 2017Article
- Elevated ventricular wall stress disrupts cardiomyocyte t-tubule structure and calcium homeostasis.Cardiovascular research · 2016Article
- Reduced immunoreactivities of B-type natriuretic peptide in pulmonary arterial hypertension rats after ranolazine treatment.Anatomy & cell biology · 2016Article
- T-tubule disruption promotes calcium alternans in failing ventricular myocytes: mechanistic insights from computational modeling.Journal of molecular and cellular cardiology · 2015Article
- AutoTT: automated detection and analysis of T-tubule architecture in cardiomyocytes.Biophysical journal · 2014Article
- CrossTalk proposal: The late sodium current is an important player in the development of diastolic heart failure (heart failure with a preserved ejection fraction).The Journal of physiology · 2014Article
- Ranolazine: Multifaceted Role beyond Coronary Artery Disease, a Recent Perspective.Heart views : the official journal of the Gulf Heart AssociationReview
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Authors and funding
18 authors at 2 institutions in 1 country.
Funding
Abstract
The treatment of heart failure (HF) is challenging and morbidity and mortality are high. The goal of this study was to determine if inhibition of the late Na(+) current with ranolazine during early hypertensive heart disease might slow or stop disease progression. Spontaneously hypertensive rats (aged 7 mo) were subjected to echocardiographic study and then fed either control chow (CON) or chow containing 0.5% ranolazine (RAN) for 3 mo. Animals were then restudied, and each heart was removed for measurements of t-tubule organization and Ca(2+) transients using confocal microscopy of the intact heart. RAN halted left ventricular hypertrophy as determined from both echocardiographic and cell dimension (length but not width) measurements. RAN reduced the number of myocytes with t-tubule disruption and the proportion of myocytes with defects in intracellular Ca(2+) cycling. RAN also prevented the slowing of the rate of restitution of Ca(2+) release and the increased vulnerability to rate-induced Ca(2+) alternans. Differences between CON- and RAN-treated animals were not a result of different expression levels of voltage-dependent Ca(2+) channel 1.2, sarco(endo)plasmic reticulum Ca(2+)-ATPase 2a, ryanodine receptor type 2, Na(+)/Ca(2+) exchanger-1, or voltage-gated Na(+) channel 1.5. Furthermore, myocytes with defective Ca(2+) transients in CON rats showed improved Ca(2+) cycling immediately upon acute exposure to RAN. Increased late Na(+) current likely plays a role in the progression of cardiac hypertrophy, a key pathological step in the development of HF. Early, chronic inhibition of this current slows both hypertrophy and development of ultrastructural and physiological defects associated with the progression to HF.
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