IMPAIRED RODENT VAGAL NERVE SODIUM-POTASSIUM-ATPASE ACTIVITY IN STREPTOZOTOCIN DIABETES

Experimental diabetes in rodents is associated with diminished activit y of sodium-potassium-adenosine triphosphatase (Na+-K+-ATPase) in the sciatic nerve, an abnormality that has been invoked as being factorial in the genesis of diabetic peripheral neuropathy. Whether a parallel metabolic abnormality occurs in the autonomic vagus nerve is unknown. To answer this question, adult male rats made diabetic with streptozot ocin (45 mg/kg) and age-matched nondiabetic controls were killed at 1 and 3 months after induction of diabetes. The cervical vagi and sciati c nerves were excised, weighed, and homogenized, and Na+-K+-ATPase act ivities were determined. After 1 month, the diabetic animals showed a significantly reduced sciatic nerve Na+-K+-ATPase activity as compared with respective controls, whether expressed in micromoles per gram we t weight per hour (20.5 +/- 4.9 [mean +/- SEM] vs 61.6 +/- 13.0) or mi cromoles per milligram of protein per hour (0.77 +/- 0.21 vs 2.48 +/- 0.57, p < 0.05, diabetic vs control, respectively). Diabetic vagus ner ve Na+-K+-ATPase activity was also diminished (40.6 +/- 6.9 mu mol/gm wet weight per hour vs 63.2 +/- 9.7 mu mol/gm wet weight per hour and 3.83 +/- 0.81 mu mol/mg protein per hour vs 5.86 +/- 0.73 mu mol/mg pr otein per hour), but the results did not reach statistical significanc e. After 3 months, diabetic sciatic nerve Na+-K+-ATPase activity was s till significantly less than the control group value (16.89 +/- 3.91 m u mol/gm wet weight per hour vs 38.9 +/- 4.24 mu mol/gm wet weight per hour and 0.48 +/- 0.11 mu mol/mg protein per hour vs 1.04 +/- 0.14 mu mol/mg protein per hour; p < 0.05, diabetic vs control, respectively) . In addition, diabetic vagus nerve Na+-K+-ATPase activity was also si gnificantly reduced (14.67 +/- 3.80 mu mol/gm wet weight per hour vs 3 8.00 +/- 5.79 mu mol/gm wet weight per hour and 0.57 +/- 0.14 mu mol/m g protein per hour vs 1.76 +/- 0.39 mu mol/mg protein per hour; p < 0. 05, diabetic vs control, respectively). These observations show that v agus nerve Na+-K+-ATPase activity is impaired in experimental diabetes mellitus. However, vagus nerve Na+-K+-ATPase activity appears to be l ess sensitive to the effects of diabetes mellitus than respective scia tic nerve activity.