Abstract
Summary Angiotensin II (All) increased the evoked release of [3H]- norepinephrine (NE) from superfused slices of interscapular fat (ISF). To determine if All was endogenously formed and subsequently released from ISF, immunoreactive All was measured in the superfusate from ISF slices. The concentration of All detected in the ISF superfusate was 4.51 pg/mg tissue wet wt/30ml collected over a 30-min period. In response to electrical field stimulation, All concentration in the superfusate increased (maximum of 2-fold). To determine if All modulates sympathetic neurotransmission, the effect of All (O.l-lOnM) and, in separate experiments the effect of the AII-1 receptor antagonist DuP 753 (1 nM-1µM) on the evoked release of [3H]-NE were examined in ISF slices. All 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 All enhances the evoked release of [3H]-NE from ISF. Keywords Brown Adipose Tissue Atrial Natriuretic Peptide Electrical Field Stimulation Krebs Buffer Neuronal Uptake These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.