In three groups of rats: control animals (n=18), hypothyroid (TX) rats (n=21) 8-10 weeks after i. p. injection of Na131I (0.4-1 mCi), and hypothyroid rats (n=16) substituted with thyroxine (TX+T3, 50 μg/kg B.W. for 7 days) proximal tubule fluid reabsorption, and transtubular concentration difference of3H-l-histidine and3H-glycodiazine at zero net flux were measured. The effectiveness of TX was confirmed by delayed growth (200±12 as compared to 400±42 g B. W.), diminished plasma concentration of thyroxine (8.0 as compared to 53 μg/l), and increased plasma concentration of TSH (0.75 as compared to 0.15 mg/l). Half time of proximal tubule reabsorption, as measured by the technique of split droplet, was increased (45.8±3.0 s as compared to 18.1±1.0 s in controls). The difference in absolute values of proximal fluid reabsorption was even more marked (1.3±0.1 as compared to 4.7±2.3·10-2 nl·s-1·mm-1) since tubule radius was smaller in TX rats (15.6±0.2 μm) than in controls (19.3±0.5 μm). Substitution with T3 for 7 days did not significantly increase tubule radius (15.7±0.2 μm). Half time of fluid reabsorption, however, was completely normalized (19.4±1.2 s) and thus, absolute value of fluid reabsorption partially restored (3.0±0.2·10-2 nl· mm-1·s-1). The concentration difference of3H-l-histidine (Cperitub-Ctubulc:Cperitub.) was 0.80±0.03 in controls and significantly decreased in TX rats (0.66±0.03). Administration of T3 to TX rats completely restored histidine reabsorption (0.80±0.03). The concentration difference for3H-glycodiazine in controls (0.84±0.01) was higher than in TX rats (0.81±0.01) and this small difference was restored by T3 administration (0.85±0.01). The data indicate that hypothyroidism strongly affects proximal fluid reabsorption and sodium coupled l-histidine transport and far less the transport of glycodiazine buffer. This suggests that thyroid hormone acts mainly on proximal tubule Na+-K+-activated ATPase. © 1980 Springer-Verlag.
Tubular transport processes in proximal tubules of hypothyroid rats - Micropuncture studies on isotonic fluid, amino acid and buffer reabsorption
CAPASSO, Giovambattista;
1980
Abstract
In three groups of rats: control animals (n=18), hypothyroid (TX) rats (n=21) 8-10 weeks after i. p. injection of Na131I (0.4-1 mCi), and hypothyroid rats (n=16) substituted with thyroxine (TX+T3, 50 μg/kg B.W. for 7 days) proximal tubule fluid reabsorption, and transtubular concentration difference of3H-l-histidine and3H-glycodiazine at zero net flux were measured. The effectiveness of TX was confirmed by delayed growth (200±12 as compared to 400±42 g B. W.), diminished plasma concentration of thyroxine (8.0 as compared to 53 μg/l), and increased plasma concentration of TSH (0.75 as compared to 0.15 mg/l). Half time of proximal tubule reabsorption, as measured by the technique of split droplet, was increased (45.8±3.0 s as compared to 18.1±1.0 s in controls). The difference in absolute values of proximal fluid reabsorption was even more marked (1.3±0.1 as compared to 4.7±2.3·10-2 nl·s-1·mm-1) since tubule radius was smaller in TX rats (15.6±0.2 μm) than in controls (19.3±0.5 μm). Substitution with T3 for 7 days did not significantly increase tubule radius (15.7±0.2 μm). Half time of fluid reabsorption, however, was completely normalized (19.4±1.2 s) and thus, absolute value of fluid reabsorption partially restored (3.0±0.2·10-2 nl· mm-1·s-1). The concentration difference of3H-l-histidine (Cperitub-Ctubulc:Cperitub.) was 0.80±0.03 in controls and significantly decreased in TX rats (0.66±0.03). Administration of T3 to TX rats completely restored histidine reabsorption (0.80±0.03). The concentration difference for3H-glycodiazine in controls (0.84±0.01) was higher than in TX rats (0.81±0.01) and this small difference was restored by T3 administration (0.85±0.01). The data indicate that hypothyroidism strongly affects proximal fluid reabsorption and sodium coupled l-histidine transport and far less the transport of glycodiazine buffer. This suggests that thyroid hormone acts mainly on proximal tubule Na+-K+-activated ATPase. © 1980 Springer-Verlag.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
