Enhanced Na-K ATPase activity in the aorta may explain the unaltered contractile responses to KCl in diabetes mellitus.

Sodium-potassium ATPase activity and transmembrane calcium influx in the aortic smooth muscle from control and diabetic rats were assessed indirectly through the measurement of KCl relaxation and contractile responses to CaCl2 in attempts to explain the contractile responses to KCl following streptozotocin-induced diabetes mellitus. There were no significant changes in the maximum contractile responses of the aortas from 4 and 12 week diabetic rats to KCl even when significant increases in calcium influx were demonstratable. On the other hand, the diabetic aortas were significantly (P < 0.05) more sensitive to KCl-induced relaxations than the controls. This provides an indirect evidence for increased activity of the sodium-postassium ATPase enzyme in the aortas from streptozotocin diabetic rats. This may, atleast in part, explain the inability of KCl to produce greater than normal contractions of the aortas from diabetic rats.