Early development of intracellular calcium cycling defects in intact hearts of spontaneously hypertensive rats - Wikidata - wikimedia - TriplyDB

Early development of intracellular calcium cycling defects in intact hearts of spontaneously hypertensive rats

Early development of intracellular calcium cycling defects in intact hearts of spontaneously hypertensive rats

http://www.wikidata.org/entity/Q33708752

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Inhibition of the late sodium current slows t-tubule disruption during the progression of hypertensive heart disease in the rat.A new twist on an old idea part 2: cyclosporine preserves normal mitochondrial but not cardiomyocyte function in mini-swine with compensated heart failure Reduced mechanical efficiency in left-ventricular trabeculae of the spontaneously hypertensive rat.T-tubule disruption promotes calcium alternans in failing ventricular myocytes: mechanistic insights from computational modeling Cardiac cellular coupling and the spread of early instabilities in intracellular Ca2+.Mechanical unloading reverses transverse tubule remodelling and normalizes local Ca(2+)-induced Ca(2+)release in a rodent model of heart failure Dobutamine "stress" test and latent cardiac susceptibility to inhaled diesel exhaust in normal and hypertensive rats.Targeted sarcoplasmic reticulum Ca2+ ATPase 2a gene delivery to restore electrical stability in the failing heart Ultrastructural and cellular basis for the development of abnormal myocardial mechanics during the transition from hypertension to heart failure.Regional distribution of T-tubule density in left and right atria in dogs.Suppression of ryanodine receptor function prolongs Ca2+ release refractoriness and promotes cardiac alternans in intact hearts.Does reduced myocardial efficiency in systemic hypertensive-hypertrophy correlate with increased left-ventricular wall thickness?Cardiac myocyte alternans in intact heart: Influence of cell-cell coupling and β-adrenergic stimulation.Effect of exercise training on Ca²⁺ release units of left ventricular myocytes of spontaneously hypertensive rats.Intracellular Ca2+ waves, afterdepolarizations, and triggered arrhythmias.Increased susceptibility of spontaneously hypertensive rats to ventricular tachyarrhythmias in early hypertension.T-tubule remodeling and increased heterogeneity of calcium release during the progression to heart failure in intact rat ventricle.Mechanisms of reduced contractility in an animal model of hypertensive heart failure.Small-conductance Ca2+-activated K+ current is upregulated via the phosphorylation of CaMKII in cardiac hypertrophy from spontaneously hypertensive rats.

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Early development of intracellular calcium cycling defects in intact hearts of spontaneously hypertensive rats

http://www.wikidata.org/entity/Q33708752

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2010 nî lūn-bûn

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2010 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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Early development of intracell ...... pontaneously hypertensive rats

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Early development of intracell ...... pontaneously hypertensive rats

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Early development of intracell ...... pontaneously hypertensive rats

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AJPHEART.00623.2010

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American Journal of Physiology - Heart and Circulatory Physiology

P1476

Early development of intracell ...... pontaneously hypertensive rats

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P2093

Alan H Kadish

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C William Balke

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Gary L Aistrup

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J Andrew Wasserstrom

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James E Kelly

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Jiabo Zheng

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Mitra Veramasuneni

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Rishi Arora

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Rohan Sharma

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Sunil Kapur

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P2860

Pacing-induced heterogeneities in intracellular Ca2+ signaling, cardiac alternans, and ventricular arrhythmias in intact rat heart.

Acidosis and ischemia increase cellular Ca2+ transient alternans and repolarization alternans susceptibility in the intact rat heart.

Abnormalities of calcium cycling in the hypertrophied and failing heart.

Age-associated changes in beta-adrenergic modulation on rat cardiac excitation-contraction coupling

Collagen remodeling of the pressure-overloaded, hypertrophied nonhuman primate myocardium.

Orphaned ryanodine receptors in the failing heart.

Perspectives on mammalian cardiovascular aging: humans to molecules.

Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: Part II: the aging heart in health: links to heart disease.

Intracellular calcium transients and developed tension in rat heart muscle. A mechanism for the negative interval-strength relationship

Cellular alternans: a mechanism linking calcium cycling proteins to cardiac arrhythmogenesis.

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10.1152/AJPHEART.00623.2010

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6

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