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Am J Physiol Regul Integr Comp Physiol 254: R33-R39, 1988;
0363-6119/88 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 254, Issue 1 33-R39, Copyright © 1988 by American Physiological Society


ARTICLES

Thyroxine, renal beta-adrenergic receptors, and dipsogenesis in food-deprived rats

L. F. Yeh, S. P. Baker and M. J. Katovich
Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville 32610.

The effect of thyroxine (T4) replacement on the increased renal beta-adrenergic receptor number and the increased beta-adrenergic dipsogenic responsiveness of fasted rats was studied in male Sprague-Dawley rats. Food deprivation significantly decreased serum thyroxine (T4) and triiodothyronine (T3) levels, increased the dipsogenic response to isoproterenol, and elevated renal beta-adrenergic receptor concentration. Daily administration of T4 (40 micrograms/kg) to food-deprived rats restored serum thyroid levels to normal. Thyroxine replacement also reduced the increased beta-adrenergic dipsogenic responsiveness in the food-deprived rats to control levels. In addition, daily administration of thyroxine reduced the beta-adrenergic receptor concentration in renal cortices to that observed in controls. Thyroid treatment tended to decrease the isoproterenol-induced renin release in food-deprived rats and increase the response in the control rats. These results suggest that the relative hypothyroid state observed in the food-deprived rat may be responsible for the increased concentration of renal beta-receptors and the associated activation of the renin-angiotensin system, which may be partially responsible for the observed increased dipsogenic response induced by isoproterenol. Collectively, the data reaffirm the interaction of thyroid hormone and beta-adrenergic responsiveness, although it is of interest that, in regard to renal beta-receptors, the concentrations are decreased to normal by thyroid treatment, whereas previous studies in hypothyroid rats demonstrate an increase to normal of cardiac beta-receptors. This would suggest thyroid hormone may normalize a response in an opposite direction depending on the direction of the disturbance.





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