Studies On Hypokalemia Induced By Trimethyltin Chloride

Objective: To study the molecular mechanism of hypokalemia induced by TMT. Method: The animal model of hypokalemia was made by treating SD rats with various doses of TMT (ip). The way of plasma potassium leakage was determined by 24-hour urine potassium tests which were carried out in different time after TMT treatment (10.0mg/kgbw); The effect of TMT on potassium reassertion was assessed by measuring the Na+-K+ATPase activities in renal epidermis membrane; The influence of TMT on renal K+ channels were analyzed by patch-clamp technique; The tissular changes of kidney caused by TMT were observed with the method of pathological techique. Results: In the low and high dose groups(10.0mg/kgbw,21.5kg/kgbw), the plasma K+ level dropped quikly half an hour after TMT treatment(p<0.05)and didn't recover until the experiment ended(the 11th day from the beginning of experiment ); In the 24h-hour urine potassium tests,the urinary potassiums in 1th day,6th day and 11th day after rats were treated with TMT(10.0mg/kgbw) increased significantly in comparison with those in the controls(p<0.05).The Na+-K+ATPase activities in renal epidermis membrane depressed remarkably(p<0.01) which were checked in 1th day,6th day and 11th day after TMT treatment(10.0mg/kgbw);We had so little time in the end that we failed to study the K+ channels in kidney using patch-clamp technique. Conclusion: TMT may induce hypokalemia in SD rats. The available evidence suggest that the increase of renal patassium excretion be the main way of potassium leakage; that the decrease of Na+-K+ATPase activities in renal epidermis membrane because of TMT could result in the reabsorption failure which may be one of molecular mechanisms of the hypokalemia lead by TMT.