Indomethacin and piroxicam inhibit Na -adenosine transport in rat renal brush-border membranes
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abstract
The effects of the cyclooxygenase inhibitors, indomethacin and piroxicam, were evaluated on Na -dependent [3H]adenosine transport in rat renal brush-border membranes of the outer renal cortex of the rat. Adenosine co-transport (1-10 μM) was estimated in the presence of 0.001-10 μM indomethacin and piroxicam. Both drugs inhibited the Na -dependent transport in a dose-dependent manner with IC50 of 3.5 μM and 0.1 μM, respectively. The Na -independent transport was not modified. Preincubations carried out on the vesicles with 10-50 μM arachidonic acid increased transport in a dose-dependent manner up to 1.7 times. Whereas 50 pM to 5 μM prostaglandin E2 in the presence of indomethacin did not change carrier activity, 5 μM prostaglandin E2 increased the Na -dependent transport 1.5 times. Other prostanoid synthesis pathways were investigated with 10 μM nordihydroguaiaretic acid (lipoxygenase inhibitor), and 17-octadecynoic acid and clotrimazole (leukotriene and cytochrome P450 inhibitors). Our results demonstrated that the Na -dependent adenosine transport in brush-border membranes was inhibited by indomethacin and piroxicam, suggesting that cyclooxygenase activity might modulate this co-transport.
The effects of the cyclooxygenase inhibitors, indomethacin and piroxicam, were evaluated on Na%2b-dependent [3H]adenosine transport in rat renal brush-border membranes of the outer renal cortex of the rat. Adenosine co-transport (1-10 μM) was estimated in the presence of 0.001-10 μM indomethacin and piroxicam. Both drugs inhibited the Na%2b-dependent transport in a dose-dependent manner with IC50 of 3.5 μM and 0.1 μM, respectively. The Na%2b-independent transport was not modified. Preincubations carried out on the vesicles with 10-50 μM arachidonic acid increased transport in a dose-dependent manner up to 1.7 times. Whereas 50 pM to 5 μM prostaglandin E2 in the presence of indomethacin did not change carrier activity, 5 μM prostaglandin E2 increased the Na%2b-dependent transport 1.5 times. Other prostanoid synthesis pathways were investigated with 10 μM nordihydroguaiaretic acid (lipoxygenase inhibitor), and 17-octadecynoic acid and clotrimazole (leukotriene and cytochrome P450 inhibitors). Our results demonstrated that the Na%2b-dependent adenosine transport in brush-border membranes was inhibited by indomethacin and piroxicam, suggesting that cyclooxygenase activity might modulate this co-transport.
