Ion-regulating renal function and influence of vasopressin and its analogues on the rate and selectiveness of the urinary potassium excretion were investigated after short-term parenteral and oral potassium loading. In experiments with Wistar rats it was shown that increase in volume of orally administrated 1.25% KCl solution from 1 to 5 ml per 100 g body weight led to the proportional rise in potassium excretion. Hyperkalemia was already observed at 5 min after parenteral potassium loading, potassium excretion reached the maximum after administration of 2 ml of KCl solution per 100 g body weight. Kaliuresis induced by oral potassium load was higher and faster than after parenteral load and was followed by increase in diuresis, urinary sodium and magnesium excretion. Desmopressin and 1-deamino-Arg4-vasotocin prevented rise of diuresis, natriuresis and magniuresis under these conditions; 1-deamino-Arg4-vasotocin and vasopressin stimulated urinary potassium excretion during first 30 min after loading. After parenteral potassium load vasopressin analogues did not affect urinary potassium and sodium excretion. The data obtained suggest the participation of the gut in regulatory signal transduction to the kidney after potassium entering and prevention of significant changes in the internal environment.