Angiotensin-(1-7) does not affect norepinephrine neuronal uptake or catabolism in rat hypothalamus and atria

1. Since we previously reported that angiotensin-(1-7) [Ang-(1-7)] increase s or inhibits norepinephrine (NE) release in rat atria or hypothalamus, res pectively, the present work was undertaken to investigate the effect of the heptapeptide on NE neuronal uptake and metabolism in atria and hypothalamu s isolated from rats. 2. Ang II (1-10 muM) caused a decrease in neuronal NE uptake in both atria and hypothalami isolated from rats. On the contrary, tissues incubated with [H-3]NE in the presence of 0.1-10 muM Ang-(1-7) showed no modification in [H-3]NE content with respect to the control group, suggesting that the hept apeptide did not modify [H-3]NE neuronal uptake. 3. To study the effect of the heptapeptide on NE catabolism, monoamine-oxid ase (MAO) and catechol-O-methyltransferase (COMT) activities were determine d. Pretreatment of the tissue with Ang-(1-7) (0.1-1.0 muM) showed a tendenc y to diminish MAO activity in rat atria, while no significant changes were observed in hypothalamic MAO activity. Moreover, the heptapeptide (0.1-1.0 muM) did not affect central COMT activity with respect to the control group . 4. Present results allow us to conclude that Ang-(1-7) interacts with norad renergic neurotransmission by increasing or inhibiting NE release at the pe ripheral and central levels, respectively, without affecting either the neu rotransmitter neuronal uptake or catabolism.