Because of the role of intracellular Na on cardiac contractility and of the depressed isometric contractile response of the hypertrophied myocardium, the effects of pressure overload on the intracellular Na activity (a(i)Na) have been investigated in papillary muscles isolated from the ferret right ventricle. In animals subjected to pulmonary artery clipped for 1 - 2 months, right ventricle-to-body weight ratio was increased by about 39% in comparison with the control group. a(i)Na was measured in quiescent papillary muscles, by means of Na-sensitive micro-electrodes, at room temperature (19-22-degrees-C). a(i)Na values were, in the control ventricular cells, 7.8 +/- 1.1 mM (mean +/- SD; n = 20) and in the hypertrophied ones, 8.0 +/- 1.2 mM (n = 49). During superfusion by medium with a reduced extracellular Na concentration ([Na]0), a(i)Na declined in control and pressure-overloaded muscles to similar steady-state levels at a given [Na]0. a(i)Na fall was mono-exponential and was characterized by a smaller time constant in the hypertrophied group upon total withdrawal of Na0 (control 209 +/- 19 s, n = 4; hypertrophied 128 +/- 42 s, n = 6). In the absence of external K, a(i)Na increased to levels that were not significantly different between both groups. It was concluded that, in quiescent preparations, steady-state a(i)Na was not modified by the hypertrophic process. However, pressure overload induced a modification of a(i)Na regulation by a possible alteration of the sarcolemmal Na/Ca exchange, although other mechanisms, such as mitochondrial Ca transport, could be involved in the differential response to Na0 removal.
