No abstract

Quinidine, a compound thought to increase cytosolic calcium ion activity, has been found to inhibit the hydrosmotic response to vasopressin (VP) and adenosine 3',5'-cyclic monophosphate (cAMP) in the toad urinary bladder. To test whether this drug has a similar action in the mammalian nephron, the effect of quinidine on the hydraulic conductivity of the isolated perfused rabbit cortical collecting tubule (CCT) exposed to either 20 microU/ml VP or 10(-4) M 8-(p-chlorophenylthio) - adenosine 3',5' - cyclic monophosphate (8-CPT-cAMP) was studied. Quinidine had no effect on the basal water permeability of the CCT. Quinidine sulfate (10(-4) M) reduced the VP-stimulated water permeability from 280 +/- 50 X 10(-7) to 115 +/- 41 X 10(-7) cm X s-1 X atm-1 (P less than 0.05). The hydrosmotic response to 8-CPTcAMP was likewise reduced following exposure to quinidine. This effect was shown to be dose dependent. In paired experiments, inhibition of the response to 10(-4) M 8-CPTcAMP averaged 11% at 10(-6) M, 27% at 5 X 10(-6) M, 53% at 5 X 10(-5) M, and 50% at 10(-4) M quinidine. Inhibition of the response to 8-CPTcAMP was estimated to be half maximal at approximately 5 X 10(-6) M quinidine. Tubules were protected against the quinidine-induced inhibition by the addition of 6.5 X 10(-5) M quin 2-acetoxymethylester in the presence of low peritubular Ca concentration. These results are consistent with the view that elevated cytosolic Ca ion levels inhibit the increase in water permeability elicited by VP or exogenous cAMP in the mammalian CCT.

No abstract

Thyroxine (10 µg/g b.w., s.c), injected either on days 2, 3 and 4 or days 8, 9 and 10, resulted in a higher a.m.–p.m. plasma corticosterone difference on day 23, compared to the vehicle-treated controls. In a separate experiment the same dose of thyroxine on days 8, 9 and 10 caused an earlier appearance of significantly higher p.m. than a.m. plasma corticosterone levels (day 15 vs day 18 in vehicle-treated controls), and earlier eye-opening (12.38 ± 0.11 thyroxine vs l5.36±O.l4 days, vehicle). These results suggest that thyroxine influences the maturation of those neural structures which participate in the regulation of the diurnal rhythm of ACTH secretion and, as a consequence, in that of corticosterone production.

No abstract