Norepinephrine stores in electrically driven guinea pig isolated atria were loaded with [3H] norepinephrine, and norepinephrine release was deduced from the radioactivity efflux. Electrical field stimulation of sympathetic nerve endings was applied during the refractory period of atrial contractions. The stimulation-induced release of norepinephrine was increased by angiotensin II (Ang II) (10−8 to 10−6 mol/L) in a concentration-dependent manner. The maximum observed effect was a 55% augmentation. The effects of 10−7 and 10−6 mol/L Ang II were abolished by 10−6 and 10−5 mol/L of the subtype I Ang II receptor antagonist losartan, respectively. Losartan by itself (10−6 mol/L) caused a 14% reduction of norepinephrine release. The subtype 2 Ang II receptor ligand PD 123319 (l−[[4-(dimethylamino)-3- methylphenyl] methyl] −5-(diphenylacetyl)-4,5,6,7-tetrahydro-l/H-imidazo [4,5 -c]pyridine-6-carboxylic acid ditrifluoroacetate) in a concentration of 10−4 mol/L had no detectable influence on transmitter release and did not antagonize the effect of Ang II. Angiotensin I (10−6 and 10−5 mol/L) increased norepinephrine release maximally by 23%. This effect was antagonized by 10−5 mol/L losartan and did not appear in the presence of 10−6 mol/L of the converting enzyme inhibitor ramiprilat. These results suggest that Ang II increases norepinephrine release by an activation of subtype 1 receptors, whereas angiotensin I is converted to Ang II to become effective.