Abstract
Several studies are reviewed in which behavioral aspects of angiotensin (Ang) II on fluid intake have been compared with induction of the immediate early gene product, Fos, as a marker of neuronal activation in rat bain. Either peripheral or central administration of Ang II induced Fos along the lamina terminalis (SFO, MnPO, AV3V) and in the magnocellular neurosecretory groups (SO, PVH). A similar pattern is seen with central injection of renin. Both pharmacological and antisense oligonucleotide probe studies indicate that an AT 1 receptor is involved, probably with the initial transduction in the SFO. Treatments that induce sodium appetite all induce Fos along the lamina terminalis, but usually 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 bradykinin which is manifest in the presence of acute captopril remains unaffected by chronic administration. This suggests that the sodium appetite that appears with chronic captopril treatment may depend in part on peptides other than Ang.
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