Vasopressin which is an antidiuretic hormone in human body produced the diuretic action in dog. This study was investigated in order to certify the diuretic action and to search out the mechanism of the action on the vasopressin. Vasopressin, when given in a dose of 10.0mU/kg, bolus+1.0mU/kg/min intravenously, exhibited the increase of urine flow(Vol), renal plasma flow(RPF), osmolar clearance (Cosm) and amounts of sodium and potassium excreted in urine ($E_{Na},;E_K$), the decrease of reabsorption rate of sodium and potassium in renal tubules ($R_{Na},;R_K$), and then elevated the mean arterial pressure(MAP). Vasopressin given in a increased dose to 30.0mU/kg, bolus+1.0mU/kg/min intravenously elicited the same aspect with that exhibited by a small dose in changes of Vol. and all renal function and potentiated the change rates, whereas this time MAP did not change at all when compared with control value. Vasopressin, when administered into a renal artery, did not induce the changes of Vol and all renal function in experimental (administered) kidney, but increased slightly the Vol, glomerular filtration rate(GFR), $E_{Na},;and;E_K$ expected the no change of $R_{Na};and;R_K$ in the control (not administered) kidney. Vasopressin, when infused into carotid artery, showed the increase of Vol. GFR, $E_{Na},;and;E_K$ and no change of $R_{Na};and;R_K$ in a dose of 1/5 of intravenous dose. Diuretic action of vasopressin administered into carotid artery was not influenced by renal denervation. Above results suggest that vasopressin produced diuretic action by hemodynamic changes in dogs. These hemodynamic changes may be mediated by central endogenous substances not associated with renal nerve.