Sodium-dependent adenosine transport is diminished in brush border membrane vesicles from hypothyroid rat kidney
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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 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 (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 -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 affinity remained unchanged (K(Na ) 11.5 ± 3.5 in N, vs K(Na ) 12.72 ± 0.7 mmol/l in Tx). Inhibition of Na -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 -dependent ADO cotransport contributes to the diminished tubular reabsorption that occurs in hypothyroidism.
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.
