Angiotensin-(1?7) Does Not Affect Norepinephrine Neuronal Uptake or Catabolism in Rat Hypothalamus and Atria

GIRONACCI M; RODRIGUEZ FERMEPIN M; VATTA MS; FERNADEZ BE; RUBIO M; PEÑA C

CELLULAR AND MOLECULAR NEUROBIOLOGY.

SPRINGER/PLENUM PUBLISHERS

Lugar: New York; Año: 2000 vol. 20 p. 773 - 779

0272-4340

1. Since we previously reported that angiotensin-(1?7) [Ang-(1?7)] increases or inhibitsnorepinephrine (NE) release in rat atria or hypothalamus, respectively, the presentwork was undertaken to investigate the effect of the heptapeptide on NE neuronal uptakeand metabolism in atria and hypothalamus isolated from rats.2. Ang II (1?10 M) caused a decrease in neuronal NE uptake in both atria and hypothalamiisolated from rats. On the contrary, tissues incubated with [3H]NE in the presenceof 0.1?10 M Ang-(1?7) showed no modification in [3H]NE content with respect to thecontrol group, suggesting that the heptapeptide did not modify [3H]NE neuronal uptake.3. To study the effect of the heptapeptide on NE catabolism, monoamine-oxidase(MAO) and catechol-O-methyltransferase (COMT) activities were determined. Pretreatmentof the tissue with Ang-(1?7) (0.1?1.0 M) showed a tendency to diminish MAOactivity in rat atria, while no significant changes were observed in hypothalamic MAOactivity. Moreover, the heptapeptide (0.1?1.0 M) did not affect central COMT activitywith respect to the control group.4. Present results allow us to conclude that Ang-(1?7) interacts with noradrenergic neurotransmissionby increasing or inhibiting NE release at the peripheral and central levels,respectively, without affecting either the neurotransmitter neuronal uptake or catabolism.