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Am J Physiol Heart Circ Physiol 272: H1589-H1597, 1997;
0363-6135/97 $5.00
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AJP - Heart and Circulatory Physiology, Vol 272, Issue 4 1589-H1597, Copyright © 1997 by American Physiological Society

ARTICLES

Thyroid status and regulation of intracellular sodium in rabbit heart

M. M. Doohan, D. F. Gray, L. C. Hool, B. G. Robinson and H. H. Rasmussen
Department of Cardiology, Royal North Shore Hospital, and University of Sydney, New South Wales, Australia.

To examine the effect of thyroid status on the homeostatic control of intracellular Na+, we studied the effect of treatment of hypothyroid rabbits with 3,5,3'-triiodothyronine (T3). Intracellular Na+ and pH (pHi) in papillary muscles and Na+-K+ pump current (Ip) in ventricular myocytes were measured with ion-sensitive microelectrode and whole cell patch-clamp techniques. Na+ influx, estimated from the rate of increase in intracellular Na+ on sudden Na+-K+ pump blockade with dihydroouabain, and Na+ efflux, calculated from Ip, were similar. Treatment with T3 induced an increase in both Na+ influx and Ip. The treatment-induced increase in Na+ influx was eliminated by 5-(N,N-dimethyl)amiloride (DMA) but not by tetrodotoxin. Treatment with T3 increased the rate of fall in pHi on exposure of the papillary muscles to DMA; when the buffer capacity was taken into account, the T3 treatment-induced increase in this rate corresponded well with the treatment-induced, DMA-inhibitable estimate of Na+ uptake. We conclude that thyroid hormone enhances both Na+-H+ exchange-mediated Na+ uptake and Na+-K+ pump-mediated Na+ efflux.


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