trans-aortic constriction induced hypertrophy Dotaz Zobrazit nápovědu
Alterations in ion channel expression and function known as "electrical remodeling" contribute to the development of hypertrophy and to the emergence of arrhythmias and sudden cardiac death. However, comparing current density values - an electrophysiological parameter commonly utilized to assess ion channel function - between normal and hypertrophied cells may be flawed when current amplitude does not scale with cell size. Even more, common routines to study equally sized cells or to discard measurements when large currents do not allow proper voltage-clamp control may introduce a selection bias and thereby confound direct comparison. To test a possible dependence of current density on cell size and shape, we employed whole-cell patch-clamp recording of voltage-gated sodium and calcium currents in Langendorff-isolated ventricular cardiomyocytes and Purkinje myocytes, as well as in cardiomyocytes derived from trans-aortic constriction operated mice. Here, we describe a distinct inverse relationship between voltage-gated sodium and calcium current densities and cell capacitance both in normal and hypertrophied cells. This inverse relationship was well fit by an exponential function and may be due to physiological adaptations that do not scale proportionally with cell size or may be explained by a selection bias. Our study emphasizes the need to consider cell size bias when comparing current densities in cardiomyocytes of different sizes, particularly in hypertrophic cells. Conventional comparisons based solely on mean current density may be inadequate for groups with unequal cell size or non-proportional current amplitude and cell size scaling.
- Klíčová slova
- L-type calcium and sodium current density, Ventricular and Purkinje myocyte, bias, cell capacitance, cell size, trans-aortic constriction induced hypertrophy,
- MeSH
- kardiomegalie * metabolismus patologie MeSH
- kardiomyocyty * metabolismus patologie MeSH
- metoda terčíkového zámku MeSH
- myši MeSH
- velikost buňky * MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Atrophy of the rat heart induced by hemodynamic unloading after heterotopic transplantation is associated with impaired relaxation while systolic function remains normal when compared to the heart of the recipient animal. To identify possible underlying mechanisms for the above, we studied some aspects of membrane calcium handling using postextrasystolic potentiation of contractions in the isolated right ventricular papillary muscle and in the left ventricle of the Langendorff-perfused heart. We also compared the alterations of the unloaded heart with those of overloaded hypertrophic hearts of rats with suprarenal aortic constriction. In the atrophic heart the degree of potentiation after one extrasystole, considered to be proportional to the trans-sarcolemmal influx of Ca2+ during an action potential, was increased by 125% when compared with recipient hearts. The rate of decay of potentiation which reflects the fraction of activator Ca2+ recirculating in the cells via the sarcoplasmic reticulum, negatively correlated with the degree of potentiation, although its mean value was not significantly altered. In hypertrophic hearts the decay of potentiation was faster when compared with the hearts of sham-operated animals, indicating a decreased recirculating fraction of Ca2+ The data suggest that the relative importance of trans-sarcolemmal Ca2+ fluxes is increased both in cardiac atrophy and hypertrophy; but their quantitative role in the control of cardiac contraction might differ.
- MeSH
- atrofie metabolismus patologie patofyziologie MeSH
- heterotopická transplantace MeSH
- krysa rodu Rattus MeSH
- srdeční komory metabolismus patologie patofyziologie MeSH
- transplantace srdce fyziologie MeSH
- vápník metabolismus MeSH
- velikost orgánu MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- vápník MeSH