THYROID STATUS AND REGULATION OF INTRACELLULAR SODIUM IN RABBIT HEART

To examine the effect of thyroid status on the homeostatic control of intracellular Na+, we studied the effect of treatment of hypothyroid r abbits with 3,5,3'-triiodothyronine (T-3). Intracellular Na+ and pH (p H(i)) in papillary muscles and Na+-K+ pump current (I-p) in ventricula r myocytes were measured with ion-sensitive microelectrode and whole c ell patch-clamp techniques. Na+ influx, estimated from the rate of inc rease in intracellular Na+ on sudden Na+-K+ pump blockade with dihydro ouabain, and Na+ efflux, calculated from I-p, were similar. Treatment with T-3 induced an increase in both Na+ influx and I-p. The treatment -induced increase in Na+ influx was eliminated by 5-(N,N-dimethyl)amil oride (DMA) but not by tetrodotoxin. Treatment with T-3 increased the rate of fall in pH(i) on exposure of the papillary muscles to DMA; whe n the buffer capacity was taken into account, the T-3 treatment-induce d increase in this rate corresponded well with the treatment-induced, DMA-inhibitable estimate of Na+ uptake. We conclude that thyroid hormo ne enhances both Na+-H+ exchange-mediated Na+ uptake and Na+-K+ pump-m ediated Na+ efflux.