Yeh L F, Baker S P, Katovich M J
Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville 32610.
Am J Physiol. 1988 Jan;254(1 Pt 2):R33-9. doi: 10.1152/ajpregu.1988.254.1.R33.
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.
在雄性斯普拉格-道利大鼠中，研究了甲状腺素（T4）替代对禁食大鼠肾β-肾上腺素能受体数量增加以及β-肾上腺素能饮水反应性增加的影响。食物剥夺显著降低了血清甲状腺素（T4）和三碘甲状腺原氨酸（T3）水平，增加了对异丙肾上腺素的饮水反应，并提高了肾β-肾上腺素能受体浓度。对食物剥夺的大鼠每日给予T4（40微克/千克）可使血清甲状腺水平恢复正常。甲状腺素替代还将食物剥夺大鼠中增加的β-肾上腺素能饮水反应性降低至对照水平。此外，每日给予甲状腺素可使肾皮质中的β-肾上腺素能受体浓度降至对照组观察到的水平。甲状腺治疗倾向于降低食物剥夺大鼠中异丙肾上腺素诱导的肾素释放，并增加对照大鼠中的反应。这些结果表明，在食物剥夺大鼠中观察到的相对甲状腺功能减退状态可能是肾β受体浓度增加以及肾素-血管紧张素系统相关激活的原因，这可能部分导致了观察到的异丙肾上腺素诱导的饮水反应增加。总体而言，这些数据再次证实了甲状腺激素与β-肾上腺素能反应性之间的相互作用，不过有趣的是，就肾β受体而言，通过甲状腺治疗其浓度降至正常，而先前对甲状腺功能减退大鼠的研究表明心脏β受体浓度增加至正常。这表明甲状腺激素可能根据干扰的方向使反应向相反方向恢复正常。
