To investigate pathomechanisms of the hypertension originating immediately after kidney transplantation, acute model studies were performed on binephrectomised hypertensive dogs receiving a cold-stored autograft. Comparative determinations of freely circulating renin-angiotensin und catecholamines were made after transplantation of canine and human kidneys, showing a corresponding post-anastomotic increase in plasma levels. For estimation of the vascular contractile response to the high plasma transmitter concentrations, antagonists having different pharmacological characteristics were infused in the dogs. It was found that immediately after transplantation the kidney's vasopressor system had only a moderate impact on increase in systemic and renal resistance. Using inhibitors of central sympathetic activities, also a moderate decline in blood pressure was observed, but it unfortunately led to a decrease in renal blood flow and filtration. The direct vasodilatatoric stimulation of vascular smooth muscle had no hemodynamic effects. However, the peripheral alpha-adrenergic blockade induced a marked decrease in blood pressure as well as an almost complete normalization of the elevated arteriolar tone of the graft associated with an increase in glomerular filtration. The suppression of vascular alpha-adrenergic stimulation was likewise attainable by inhibition of the neuro-muscular transmission due to calcium channel blockade. The results suggest that sympathetic vasoconstriction plays the major role in producing this type of posttransplant hypertension.