Abstract
Myocardial hyperfunction is experimentally modeled by coarctation of the aorta in mature (6–8-month-old) and senescent (26–28-month-old) Wistar rats. During the emergency phase of cardiac hyperfunction Na,K-ATPase activity is shown to rise reliably in mature animals, while in old rats it remains unchanged. Cardiomyocyte cytosol and blood plasma from mature (but not old) rats with experimental coarctation of the aorta activate Na,K-ATPase in membranes from the myocardium of both the mature and old rats. It is assumed that the activation of Na,K-ATPase during the emergency stage of cardiac hyperfunction is mediated through synthesis of specific invertors. In senescent animals the synthesis of invertors probably becomes insufficient, while membrane sensitivity to them is preserved.
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