Several studies are reviewed in which behavioral aspects of angiotensi
n (Ang) II on fluid intake have been compared with induction of the im
mediate early gene product, Fos, as a marker of neuronal activation in
rat bain. Either peripheral or central administration of Ang II induc
ed Fos along the lamina terminalis (SFO, MnPO, AV3V) and in the magnoc
ellular neurosecretory groups (SO, PVH). A similar pattern is seen wit
h central injection of renin. Both pharmacological and antisense oligo
nucleotide probe studies indicate that an AT(1) receptor is involved,
probably with the initial transduction in the SFO. Treatments that ind
uce sodium appetite all induce Fos along the lamina terminalis, but us
ually not in the SO or PVN. Kininase II inhibitors, such as captopril,
acutely potentiate drinking to Ang I, but after chronic exposure they
may inhibit water intake. In contrast, the dipsogenic effect of brady
kinin which is manifest in the presence of acute captopril remains una
ffected by chronic administration. This suggests that the sodium appet
ite that appears with chronic captopril treatment may depend in part o
n peptides other than Ang.