Role of angiotensin in the dipsogenic effect of bradykinin in rats

We have previously shown that peripheral administration of bradykinin (BK) induces water intake in rats acutely pretreated with captopril, a kininase II inhibitor. We now show that BK-induced drinking is also observed in rats treated chronically with dietary captopril, and that this is reversed by Hoe 140, a BK receptor antagonist. Both acute and chronic captopril in combination with BK caused a large increase in plasma renin activity. Fos-like immunoreactivity (Fos-in used as a marker of cellular activation) was induced by BK + captopril in regions of the brain previously associated with action of angiotensin (Ang) II, including the circumventricular organs and the magnocellular hypothalamic nuclei. However, while water intake induced by peripheral administration of Ang I was potentiated by acute administration of captopril, it was suppressed by chronic captopril treatment. Fos-IR induced in brain by Ang I was not markedly affected by either acute or chronic treatment with captopril. The simultaneous occurrence of potentiated drinking to BK and inhibited drinking to Ang I following chronic treatment with captopril suggest that different mechanisms of action are involved. In order to further examine this possibility, rats were given lesions of the anterodorsal third ventricle region. Lesions that completely abolished the water intake following administration of Ang II only partly attenuated water intake induced by BK + captopril. Further, Fos-IR induced by BK + captopril was only partly (31%) reduced in the supraoptic and paraventricular nuclei of lesioned rats compared with sham operated controls. We suggest that at least two mechanisms, one Ang-related, underlie drinking after BK+captopril.