The interrelations between angiotensin and catecholamine uptake have been studied in rats. Angiotensin was infused for either 5, 30, or 120 minutes at three dose levels: 1, 12, and 45 ng/kg/min. With short exposures to angiotensin, effects were seen in kidney, uterus, and adrenal gland. These organs had been previously shown to bind the greatest amount of tritiated peptide administered intravenously. In the 5- and 30-minute experiments angiotensin inhibited uptake of either metaraminol or norepinephrine in most tissues, especially at the higher dose levels, with the exception of the adrenal gland where uptake was increased. After the two-hour infusion inhibition of uptake was seen in most organs. When high titer angiotensin II antibodies were administered intravenously, responses to iv angiotensin were abolished. At this stage the uptake of tritiated norepinephrine was increased in kidney, heart, spleen, and vas deferens, while it was decreased in the adrenal gland. To see whether these biochemical findings are related to a physiological role, contractile responses of isolated perfused arteries of rabbits were studied. Angiotensin potentiated the increase in perfusion pressure after the infusion of norepinephrine, while angiotensin II antibodies decreased this response. Thus, it is concluded that angiotensin can modify the uptake and, hence, the inactivation of the sympathetic neurotransmitter and possibly by this mechanism alter the physiological response to norepinephrine and sympathetic stimulation.