Modulation of electrical heterogeneity by compensated hypertrophy
in rat left ventricle.
G[acute]omez, Ana Mar[acute]ia, Jean-Pierre B[acute]enitah, Daniel
Henzel, Alain Vinet, Paco Lorente, and Carmen Delgado.
Instituto de Farmacolog[acute]ia y Toxicolog[acute]ia (CSIC-UCM),
Facultad de Medicina, 28040 Madrid, Spain and U 390 INSERM, CHU
Arnaud de Villeneuve, 34295 Montpellier, France
APStracts 3:0439H, 1996.
Modulation of regional distribution of action potential by left
ventricular hypertrophy, and the role of calcium current (ICa) and
transient outward current (Ito) in the action potential duration
(APD) were investigated in normal and hypertrophied rat ventricular
myocytes from apex (A), septum (S) and left ventricular free wall
(FW) by using whole-cell current and voltage-clamp techniques.
Hypertrophy was induced by abdominal aortic constriction. In control
cells, APD measured at 20% repolarization (APD20) assumed the
shortest values in A and the longest in S, whereas FW cells showed
intermediate values. Hypertrophy significantly prolonged APD20 and
increased APD variability within A and FW regions, but did not modify
APD in S cells. Analysis of APD, ICa, and Ito at the instant of 20%
repolarization in the same cell showed that in control cells, the
shortest APD20 was associated with a prominent Ito in A and FW,
whereas long APD20 was identified with lower Ito in S myocytes.
Hypertrophy-induced prolongation of APD20 was associated with a
reduction of Ito in A and FW. Significant correlations could be
established between APD20 and the "net current" defined as
the algebraic addition of Ito and ICa in A and FW control groups, but
not in control S nor in hypertrophied cells whatever the origin of
cells. Our results indicate that inter-regional APD heterogeneity is
lost while intra-regional APD variability is increased in A and FW
during the hypertrophic process. These effects are largely due to a
change in the balance between ICa and Ito which is a major
contributing factor to the heterogeneity of the initial phase of
repolarization in normal rat ventricle.
Received 27 March 1996; accepted in final form 19 September 1996.
APS Manuscript Number H291-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996