ArticleBritish journal of pharmacology2004
Tedisamil attenuates foetal transformation of myosin in the hypertrophied rat myocardium.
Article in British journal of pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 3 citations in OpenAlex.
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3 authors at 3 institutions in 2 countries.
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Abstract
1 Reduction in repolarizing potassium currents has controversial effects on hypertrophic responses in cardiomyocytes of transgenic models and cultured cardiomyocytes. It remains thus unknown whether a blockade of potassium channels with tedisamil (N,N'dicyclopropylmethylene-9,9-tetramethylene-3,7-diazabicyclo(3.3.1)nonane dihydrochloride) has any effects on cardiac growth during postnatal development or pressure overload. 2 To test the hypothesis that a treatment with tedisamil affects cardiac growth or protein phenotype, sham-operated rats and rats with ascending aorta constriction were treated with tedisamil (36 mg kg day(-1)) for 7 weeks. Left ventricular mass and geometry, relative expression of myosin isoforms, hydroxyproline concentration and isovolumic ventricular function were assessed. 3 Rats with aortic constriction exhibited a marked increase in left ventricular weight and the diastolic pressure-volume relationship was shifted to smaller volumes. The hydroxyproline concentration remained unaltered. The proportion of alpha-myosin heavy chains was, however, reduced (P<0.05). Hypertrophied left ventricles manifested an enhanced overall performance but depressed myocardial contractility. 4 Administration of tedisamil was associated with decreased heart rate (P<0.05). In contrast, cardiac growth in sham-operated rats and concentric left ventricular hypertrophy of pressure-overloaded animals was not significantly altered. Hypertrophied hearts from rats treated with tedisamil expressed more alpha-myosin heavy chains (65+/-4 versus 57+/-4%; P<0.05). Also, maximal rate of wall stress rise and decline was higher (P<0.05) in tedisamil-treated pressure-overloaded rats. 5 In the rat model of pressure-overloaded hypertrophy, tedisamil had no effect on cardiac growth but partially corrected myocardial dysfunction. Postulated mechanism of this effect is the phenotype modification of myosin filaments in hypertrophied myocardium.
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