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Action potential and plateau ionic currents in moderately and severely DOCA-salt hypertrophied rat hearts.
J Mol Cell Cardiol. 1996 Dec; 28(12):2511-22.JM

Abstract

Ventricular hypertrophy is associated with an increase in action potential (AP) plateau amplitude and duration. In a model of cardiac hypertrophy by DOCA-pellet implantation in uninephrectomized saline-drinking rats, we have previously demonstrated that the influence of hypertrophy was to reduce Ito1 density, the process being fully reversible after elimination of DOCA pellets. In that study the decrease of Ito1 density appeared to vary from moderate reduction to complete suppression which could explain, at least in part, the AP lengthening. In the present study the effect of the degree of hypertrophy (moderate and severe hypertrophy) was investigated on rat ventricular action potential plateau amplitude and duration, high threshold calcium current, Ica-L, Na-Ca exchange current, INa-Ca, transient outward potassium current, Ito1, and sustained outward potassium current Isus. Ventricular action potentials of isolated perfused hearts were recorded by means of standard floating microelectrodes and ionic currents of single ventricular myocytes were measured using the whole-cell recording patch-clamp technique. We show that: (1) AP plateau amplitude and duration increase more markedly in severe than in moderate hypertrophy; (2) the decrease in Ito1 density is much larger in severe than in moderate hypertrophy whereas ICa-L, INa-Ca and i(sus) densities remain unaltered in either state of hypertrophy. After suppression of Ito1 by 3 mM 4-aminopyridine, action potential plateau amplitude and duration remain increased in severely hypertrophied rat hearts compared to sham rats. Therefore, although these results designate Ito1 reduction as the main cause of hypertrophy-induced AP changes, those occurring in severe hypertrophy cannot be uniquely explained by a quasi-complete extinction of Ito1.

Authors+Show Affiliations

Laboratoire de Cardiologie Moléculaire et Cellulaire (CNRS URA 1159), Hôpital Marie Lannelongue, Le Plessis Robinson, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9004167

Citation

Momtaz, A, et al. "Action Potential and Plateau Ionic Currents in Moderately and Severely DOCA-salt Hypertrophied Rat Hearts." Journal of Molecular and Cellular Cardiology, vol. 28, no. 12, 1996, pp. 2511-22.
Momtaz A, Coulombe A, Richer P, et al. Action potential and plateau ionic currents in moderately and severely DOCA-salt hypertrophied rat hearts. J Mol Cell Cardiol. 1996;28(12):2511-22.
Momtaz, A., Coulombe, A., Richer, P., Mercadier, J. J., & Coraboeuf, E. (1996). Action potential and plateau ionic currents in moderately and severely DOCA-salt hypertrophied rat hearts. Journal of Molecular and Cellular Cardiology, 28(12), 2511-22.
Momtaz A, et al. Action Potential and Plateau Ionic Currents in Moderately and Severely DOCA-salt Hypertrophied Rat Hearts. J Mol Cell Cardiol. 1996;28(12):2511-22. PubMed PMID: 9004167.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Action potential and plateau ionic currents in moderately and severely DOCA-salt hypertrophied rat hearts. AU - Momtaz,A, AU - Coulombe,A, AU - Richer,P, AU - Mercadier,J J, AU - Coraboeuf,E, PY - 1996/12/1/pubmed PY - 1996/12/1/medline PY - 1996/12/1/entrez SP - 2511 EP - 22 JF - Journal of molecular and cellular cardiology JO - J Mol Cell Cardiol VL - 28 IS - 12 N2 - Ventricular hypertrophy is associated with an increase in action potential (AP) plateau amplitude and duration. In a model of cardiac hypertrophy by DOCA-pellet implantation in uninephrectomized saline-drinking rats, we have previously demonstrated that the influence of hypertrophy was to reduce Ito1 density, the process being fully reversible after elimination of DOCA pellets. In that study the decrease of Ito1 density appeared to vary from moderate reduction to complete suppression which could explain, at least in part, the AP lengthening. In the present study the effect of the degree of hypertrophy (moderate and severe hypertrophy) was investigated on rat ventricular action potential plateau amplitude and duration, high threshold calcium current, Ica-L, Na-Ca exchange current, INa-Ca, transient outward potassium current, Ito1, and sustained outward potassium current Isus. Ventricular action potentials of isolated perfused hearts were recorded by means of standard floating microelectrodes and ionic currents of single ventricular myocytes were measured using the whole-cell recording patch-clamp technique. We show that: (1) AP plateau amplitude and duration increase more markedly in severe than in moderate hypertrophy; (2) the decrease in Ito1 density is much larger in severe than in moderate hypertrophy whereas ICa-L, INa-Ca and i(sus) densities remain unaltered in either state of hypertrophy. After suppression of Ito1 by 3 mM 4-aminopyridine, action potential plateau amplitude and duration remain increased in severely hypertrophied rat hearts compared to sham rats. Therefore, although these results designate Ito1 reduction as the main cause of hypertrophy-induced AP changes, those occurring in severe hypertrophy cannot be uniquely explained by a quasi-complete extinction of Ito1. SN - 0022-2828 UR - https://www.unboundmedicine.com/medline/citation/9004167/Action_potential_and_plateau_ionic_currents_in_moderately_and_severely_DOCA_salt_hypertrophied_rat_hearts_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2828(96)90243-6 DB - PRIME DP - Unbound Medicine ER -