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 o bserved in rats treated chronically with dietary captopril, and that t his is reversed by Hoe 140, a BK receptor antagonist. Both acute and c hronic captopril in combination with BK caused a large increase in pla sma renin activity. Fos-like immunoreactivity (Fos-ir: used as a marke r of cellular activation) was induced by BK + captopril in regions of the brain previously associated with action of angiotensin (Ang) II, i ncluding the circumventricular organs and the magnocellular hypothalam ic nuclei. However, while water intake induced by peripheral administr ation of Ang I was potentiated by acute administration of captopril, i t was suppressed by chronic captopril treatment. Fos-IR induced in bra in by Ang I was not markedly affected by either acute or chronic treat ment with captopril. The simultaneous occurrence of potentiated drinki ng to BK and inhibited drinking to Ang I following chronic treatment w ith captopril suggest that different mechanisms of action are involved . In order to further examine this possibility, rats were given lesion s of the anterodorsal third ventricle region Lesions that completely a bolished the water intake following administration of Ang II only part ly attenuated water intake induced by BK + captopril. Further, Fos-IR induced by BK + captopril was only partly (31%) reduced in the supraop tic and paraventricular nuclei of lesioned rats compared with sham ope rated controls. We suggest that at least two mechanisms, one Ang-relat ed, underlie drinking after BK + captopril. (C) 1997 Elsevier Science Inc.