Sodium-dependent adenosine transport is diminished in brush border membrane vesicles from hypothyroid rat kidney |
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Authors: | F. Martínez Martha Franco Alicia Quintana Jaime Herrera-Acosta |
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Affiliation: | (1) Department of Pharmacology, Facultad de Medicina de la UASLP, Av. Venustiano Carranza No. 2405, 78210-Los Filtros, San Luis Potosí, Mexico, MX;(2) Department of Nephrology, Instituto Nacional de Cardiologia Ignacio Chávez, Mexico City, 14080, Mexico, MX |
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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+ 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% in N as opposed to 58% in Tx with dipyridamole, and 72% in N versus 47% in Tx with PACPX. These results suggest that decreased Na+-dependent ADO cotransport contributes to the diminished tubular reabsorption that occurs in hypothyroidism. Received: 17 June 1996 / Received after revision: 9 September 1996 / Accepted: 16 September 1996 |
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Keywords: | Adenosine receptors Nucleoside transport Sodium-coupled adenosine transport Hypothyroidism Brush border |
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