INTRACELLULAR SODIUM ACTIVITY AND ITS REGULATION IN GUINEA-PIG ATRIAL MYOCARDIUM

1. Intracellular Na+ activity (a(Na)i) and membrane resting potential were studied in quiescent guinea-pig atrial and papillary muscles by means of Na+-sensitive and conventional microelectrodes. The effects of the cardioactive steroid dihydroouabain (DHO) on a(Na)i, force of contraction and sarcolemmal Na+, K+-ATPase activity were also investigated. 2. In thirty atria and twenty-two papillary muscles, a(Na)i amounted to 8.0 +/- 0.2 and 4.7 +/- 0.3 mm, respectively (means +/- S.E.M.). When both tissues were from the same animal, with the same ion-sensitive microelectrode mean a(Na)i values of 7.9 +/- 0.2 and 5.1 +/- 0.5 mm (P < 0.01) were obtained from eight atrial and eight papillary muscles, respectively. 3. Membrane resting potentials (E(m)) were significantly (P < 0.001) more negative in the papillary muscles (- 83.5 +/- 0.7 mV; n = 8) than in the atrium (- 78.1 +/- 0.5 mV; n = 8). Deviation of E(m) from E(K) (determined by K+-sensitive microelectrodes) was 3.0 +/- 0.2 mV in ventricular (P < 0.05) and 6.1 +/- 0.3 mV in atrial preparations (P < 0.05). 4. Inhibition of the Na+ pump by DHO increased a(Na)i of the atrium within 1 0 min by 0.6 +/- 0.1 (n = 7), 1.3 +/- 0.1 (n = 5) and 3.2 +/- 0.2 mm (n = 5) at 5, 10 and 30 muM, respectively. In the papillary muscle, 10 mum DHO was without effect while a(Na)i rose by 1.0 +/- 0.1 (n = 5) and 2.9 +/- 0.2 mm (n = 6) at 30 and 120 mum DHO. 5. Consistent with the a(Na)i. measurements, the potency of DHO to increase force of the isometric contraction was three times higher in atrium than in papillary muscle (stimulation frequency 0.2 Hz). 6. Hydrolytic activity of sarcolemmal Na+,K+-ATPase isolated from atria amounted to only one third of that detected in ventricles (0-07 +/- 0.01, n = 6, versus 0.2 +/- 0.01 mumol phosphate released min-1 (g tissue)-1, n = 5). The inhibitory potencies of DHO on sarcolemmal Na+,K+-ATPase preparations were found to be identical in the enzymes from either tissue. 7. It is concluded that a lower Na+ pump density is responsible for the higher a(Na)i and for the lower resting membrane potential in atrial as compared to ventricular cells. The regulation of cellular Na+ homeostasis in atrial muscle appears to be closer to the limits of its capacity than in ventricle, explaining the higher sensitivity of the atrium to interventions which impede Na+ pump activity.