AJP - Heart and Circulatory Physiology, Vol 267, Issue 5 1851-H1861, Copyright © 1994 by American Physiological Society

ARTICLES

Effect of hypertrophy on mechanisms of relaxation in isolated cardiac myocytes from guinea pig

R. U. Naqvi and K. T. Macleod
Department of Cardiac Medicine, National Heart and Lung Institute University of London, United Kingdom.

Modifications to cell relaxation and handling of intracellular Ca have been demonstrated in animals with cardiac cell hypertrophy leading to decompensated heart failure. A previously described model of renal hypertension leading to cardiac cell hypertrophy in the guinea pig, produced using the Goldblatt 2-kidney, 1-clip technique, was used to investigate which of the main mechanisms causing cell relaxation (the sarcoplasmic reticulum Ca-adenosinetriphosphatase and Na/Ca exchanger) are altered in hypertrophy. Relaxation upon rewarming from a rapid cooling contracture was slowed in hypertrophied (H) compared with control (C) cells. Relaxation was further slowed in H compared with C cells when Na/Ca exchange was inhibited by rewarming in a Na-free, Ca-free solution and slowed most markedly in H cells in the presence of 10 mM caffeine. Hypertrophy led to greater modification of cell length relaxation in comparison with the decline in the indo-1 transient, but the force-pCa relationship in skinned muscles showed that myofilament sensitivity was unchanged. Such results indicate that cell relaxation and Ca handling are affected in hypertrophy, possibly involving modifications of Na/Ca exchange activity.

This article has been cited by other articles:

				M. R. Fowler, J. R. Naz, M. D. Graham, G. Bru-Mercier, S. M. Harrison, and C. H. Orchard Decreased Ca2+ extrusion via Na+/Ca2+ exchange in epicardial left ventricular myocytes during compensated hypertrophy Am J Physiol Heart Circ Physiol, May 1, 2005; 288(5): H2431 - H2438. [Abstract] [Full Text] [PDF]

				S. Y. Boateng, R. U. Naqvi, M. U. Koban, M. H. Yacoub, K. T. MacLeod, and K. R. Boheler Low-dose ramipril treatment improves relaxation and calcium cycling after established cardiac hypertrophy Am J Physiol Heart Circ Physiol, March 1, 2001; 280(3): H1029 - H1038. [Abstract] [Full Text] [PDF]

				J.-M. Pei, J.-J. Zhou, J.-S. Bian, X.-C. Yu, M.-L. Fung, and T.-M. Wong Impaired [Ca2+]i and pHi responses to kappa -opioid receptor stimulation in the heart of chronically hypoxic rats Am J Physiol Cell Physiol, November 1, 2000; 279(5): C1483 - C1494. [Abstract] [Full Text] [PDF]

				S. R. Shorofsky, R. Aggarwal, M. Corretti, J. M. Baffa, J. M. Strum, B. A. Al-Seikhan, Y. M. Kobayashi, L. R. Jones, W. G. Wier, and C. W. Balke Cellular Mechanisms of Altered Contractility in the Hypertrophied Heart : Big Hearts, Big Sparks Circ. Res., March 5, 1999; 84(4): 424 - 434. [Abstract] [Full Text] [PDF]

				R. L. Skolnick, S. E. Litwin, W. H. Barry, and K. W. Spitzer Effect of ANG II on pHi, [Ca2+]i, and contraction in rabbit ventricular myocytes from infarcted hearts Am J Physiol Heart Circ Physiol, November 1, 1998; 275(5): H1788 - H1797. [Abstract] [Full Text] [PDF]

				L. S. Maier, R. Brandes, B. Pieske, and D. M. Bers Effects of left ventricular hypertrophy on force and Ca2+ handling in isolated rat myocardium Am J Physiol Heart Circ Physiol, April 1, 1998; 274(4): H1361 - H1370. [Abstract] [Full Text] [PDF]