Clinically, the administration of quinidine to digitalized patients results in an elevation of serum digoxin concentration. It has been suggested that quinidine displaces tissue-bound digoxin and that renal digoxin clearance is reduced. We studied the influence of digoxin-quinidine interaction on 125l-digoxin uptake by various rat tissues in vitro, employing the tissue slice method. S/M digoxin ratios were kidney 1.72 ± 0.24 (mean ± S.D.), heart 2.36 ± 0.31, muscle 2.05 ± 0.21 (n = 23 for each), and fat 0.25 ± 0.10 (n = 9). Addition of quinidine to the incubation medium resulted in a 17.4% reduction of digoxin uptake by kidney tissue to 1.42 ± 0.38 (n = 24) (p < 0.01). Quinidine failed to reduce digoxin uptake in both heart and striated muscle. Metabolic blockade resulted in a significant reduction in digoxin uptake in kidney slices from 1.93 ± 0.23 to 1.34 ± 0.18 with DNP (n = 10) and to 1.30 ± 0.15 (n = 10) with sodium azide (p < 0.001). Digoxin uptake in either heart or muscle was uninfluenced by metabolic blockers. We conclude that active energy-dependent transport mechanism for digoxin exists in renal cortical tissue. This mechanism is inhibited by either quinidine or metabolic blockers. In contrast, uptake in heart or muscle represents a different transport mechanism unaffected by quinidine or metabolic blockers.
|Number of pages||5|
|Journal||Journal of Laboratory and Clinical Medicine|
|State||Published - 1980|
- S/M ratio
- slice-to-medium ratio
- sodium-potassium adenosine triphosphatase