Presynaptic modulation of neurotransmitter release by endogenous angiotensin II in brown adipose tissue

Angiotensin II (AII) increased the evoked release of [3H]-norepinephrine (NE) from superfused slices of interscapular fat (ISF). To determine if AII was endogenously formed and subsequently released from ISF, immunoreactive AII was measured in the superfusate from ISF slices. The concentration of AII detected in the ISF superfusate was 4.51 pg/mg tissue wet wt/30 ml collected over a 30-min period. In response to electrical field stimulation, AII concentration in the superfusate increased (maximum of 2-fold). To determine if AII modulates sympathetic neurotransmission, the effect of AII (0.1-10 nM) and, in separate experiments the effect of the AII-1 receptor antagonist DuP 753 (1 nM-1 microM) on the evoked release of [3H]-NE were examined in ISF slices. AII and DuP 753 increased (100% above control) and decreased (43% of control), respectively, the evoked [3H]-NE release from ISF slices. The effect of DuP 753 was not altered by the inclusion of neuronal uptake inhibitors (nomifensine or desipramine) in the superfusion buffer. These results suggest that endogenous AII enhances the evoked release of [3H]-NE from ISF.