Sodium-dependent adenosine transport is diminished in brush border membrane vesicles from hypothyroid rat kidney Article uri icon

abstract

  • Studies of the uptake of [3H]adenosine ([3H]-ADO) were performed using brush border membrane vesicles (BBMV) from normal (N) and hypothyroid (Tx) rat kidneys, to test if decreased Na%2b reabsorption in hypothyroidism might be associated with abnormalities in ADO transport. [3H]ADO uptake (1-10 μmol) for both conditions was measured in the presence of Na%2b (10-150 mmol/l); the effects of dipyridamole (10 μmol/l and 1,3-dipropyl-8-(2-amino-4-chlorophenyl)xanthine (PACPX, 10 μmol/l) were also studied. Na%2b-stimulated ADO uptake was decreased in Tx BBMV. Michaelis-Menten constants showed a decreased ADO carrier affinity (K(m) 2.46 ± 0.14 in N, vs K(m) 4.46 ± 0.88 μmol/l in Tx, P < 0.05), with no change in the number of carriers (V(max) 295 ± 25 in N, vs 229.2 ± 56 pmol · min-1 · mg protein in Tx). Na%2b affinity remained unchanged (K(Na%2b) 11.5 ± 3.5 in N, vs K(Na%2b) 12.72 ± 0.7 mmol/l in Tx). Inhibition of Na%2b-dependent ADO transport was 50%25 in N as opposed to 58%25 in Tx with dipyridamole, and 72%25 in N versus 47%25 in Tx with PACPX. These results suggest that decreased Na%2b-dependent ADO cotransport contributes to the diminished tubular reabsorption that occurs in hypothyroidism.

publication date

  • 1996-01-01