Thyroid status and regulation of intracellular sodium in rabbit
heart.
Doohan, Melissa M., David F. Gray, Livia C. Hool, Bruce G. Robinson,
and Helge H. Rasmussen.
Departments of Cardiology and Endocrinology, Royal North Shore
Hospital, St. Leonards, and University of Sydney, New South Wales,
Australia
APStracts 3:0502H, 1996.
To examine the effect of thyroid status on homeostatic control of
intracellular Na+ we studied the effect of treatment of hypothyroid
rabbits with 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+ upon 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 upon exposure of 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.
Received 3 October 1995; accepted in final form 21 November 1996.
APS Manuscript Number H929-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996