A direct relationship between plasma aldosterone and cardiac L-type Ca2+ current in mice

Détails

ID Serval
serval:BIB_099B7B7B82E7
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
A direct relationship between plasma aldosterone and cardiac L-type Ca2+ current in mice
Périodique
Journal of Physiology
Auteur(s)
Perrier R., Richard S., Sainte-Marie Y., Rossier B. C., Jaisser F., Hummler E., Bénitah J. P.
ISSN
0022-3751
Statut éditorial
Publié
Date de publication
11/2005
Peer-reviewed
Oui
Volume
569
Numéro
Pt 1
Pages
153-62
Notes
Journal Article --- Old month value: Nov 15
Résumé
Aldosterone is involved in a variety of pathophysiological processes that ultimately cause cardiovascular diseases. Despite this, the physiological role of aldosterone in heart function remains elusive. We took advantage of transgenic mouse models characterized by a renal salt-losing (SL) or salt-retaining (SR) phenotype, thus exhibiting chronically high or low plasma aldosterone levels, respectively, to investigate the chronic effects of aldosterone in cardiomyocytes devoid of pathology. On a diet containing normal levels of salt, these animals do not develop any evidence of cardiovascular disease. Using the whole cell patch-clamp technique on freshly isolated adult ventricular cardiomyocytes, we observed that the amplitude of L-type Ca(2)(+) currents (I(Ca)) correlates with plasma aldosterone levels. Larger values of I(Ca) are associated with high aldosterone concentrations in SL models, whereas smaller values of I(Ca) were observed in the SR model. Neither the time- nor the voltage-dependent properties of I(Ca) varied measurably. In parallel, we determined whether modulation of I(Ca) by blood concentration of aldosterone has a major physiological impact on the excitation-contraction coupling of the cardiomyocytes. Action potential duration, [Ca(2)(+)](i) transient amplitude and contraction are increased in the SL model and decreased in the SR model. In conclusion, we demonstrate that the blood concentration of aldosterone exerts chronic regulation of I(Ca) in mouse cardiomyocytes. This regulation has important consequences for excitation-contraction coupling and, potentially, for other Ca(2)(+)-regulated functions in cardiomyocytes.
Mots-clé
Aldosterone/*blood Animals Calcium/*metabolism Calcium Channels, L-Type/*physiology Calcium Signaling/*physiology Cells, Cultured Female Ion Channel Gating/*physiology Male Membrane Potentials/*physiology Mice Mice, Inbred C57BL Mice, Transgenic Myocytes, Cardiac/*physiology Statistics as Topic
Pubmed
Web of science
Création de la notice
24/01/2008 14:00
Dernière modification de la notice
20/08/2019 13:31
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