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Title: Thyroid status and regulation of intracellular sodium in rabbit heart. Author: Doohan MM, Gray DF, Hool LC, Robinson BG, Rasmussen HH. Journal: Am J Physiol; 1997 Apr; 272(4 Pt 2):H1589-97. PubMed ID: 9139940. Abstract: 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.[Abstract] [Full Text] [Related] [New Search]