Can changes in sarcolemmal membranes account for the altered inotropic responsiveness in hypertrophied heart?

Hypertrophy is an adaptive mechanism of the heart subjected to pressure overload. Ultrastructural, electrophysiological and mechanical changes occur during this adaptation. A decrease in the inotropic responsiveness of the hypertrophied heart has often been observed as compared to the normal heart. Four sarcolemmal mechanisms that could account for this modification have been described. The mechanism of action of each system (calcium channel, alpha-and beta-adrenergic systems, (Na+,K+)-ATPase) of the hypertrophied heart has been compared to that of the normal heart. In spite of the paucity of results available relating to the calcium channel, the lengthening of the action potential in every case of compensatory hypertrophy could be explained by an altered functioning of the calcium channel. alpha- and beta-adrenergic systems in the hypertrophied heart could be modified at the receptor level itself, or at another level in the cascade of events under their control. For example, two different models of hypertrophy showed a decreased inotropic responsiveness correlated to a defect in the GS regulatory protein. The modification of the ouabain-receptor (Na+,K+)-ATPase mediates a decrease and a prolongation of the inotropic response. According to the modifications of each system, a direct relationship does not seem to exist between the stimulated membrane system and the inotropic responsiveness of the hypertrophied heart.