Cellular distribution of calcium current is unaltered during compensated hypertrophy in the spontaneously hypertensive rat

Fowler, M.R., Orchard, C.H. and Harrison, S.M. (2007) Cellular distribution of calcium current is unaltered during compensated hypertrophy in the spontaneously hypertensive rat. Pflügers Archiv - European Journal of Physiology, 453(4), pp. 463-469. (doi: 10.1007/s00424-006-0147-5)

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Abstract

Changes in cellular calcium (Ca2+) handling are thought to underlie the altered contraction that occurs during cardiac hypertrophy and failure. Recent work has highlighted the importance of t-tubules in the control of intracellular Ca2+. The present study was performed to investigate whether changes in the distribution of I Ca between the surface and t-tubule membranes might contribute to the altered Ca2+ handling observed during compensated hypertrophy in the spontaneously hypertensive rat (SHR). Experiments were performed on ventricular myocytes isolated from 5-month-old SHR and normotensive Wistar-Kyoto (WKY) control rats. Osmotic shock using formamide was used to disrupt the t-tubular system and the whole-cell patch clamp technique used to monitor I Ca in the presence and absence of t-tubules. Membrane capacitance and I Ca were greater in control SHR than WKY myocytes; following detubulation, cell capacitance and I Ca both decreased and were no longer significantly different in the two cell types. The density of I Ca was not significantly different in control SHR and WKY cells or in detubulated myocytes from the two species. These data suggest that the distribution of I Ca is unchanged in SHR myocytes compared to WKY controls; I Ca density in the t-tubules was 1.2-fold greater than in the sarcolemma in both strains. These data also imply that the increase in surface area in SHR myocytes is due principally to an increase in t-tubular area, which is accompanied by an approximately equivalent increase in I Ca, so that the density of I Ca at the cell surface and in the t-tubules remains the same. These changes would be expected to retain cell function and synchronicity of Ca2+ release in the SHR at this stage of compensated hypertrophy.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Fowler, Dr Mark
Authors: Fowler, M.R., Orchard, C.H., and Harrison, S.M.
College/School:College of Medical Veterinary and Life Sciences
Journal Name:Pflügers Archiv - European Journal of Physiology
Publisher:Springer-Verlag
ISSN:0031-6768
ISSN (Online):1432-2013
Published Online:26 October 2006

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