Elevated salt appetite and brain binding of angiotensin II in mineralocorticoid-treated rats.

Angiotensin II (Ang II) and aldosterone levels increase with sodium deficiency, promoting sodium conservation and arousing a salt appetite in rats. The mechanism(s), by which these two hormones interact to produce salt appetite is not known. The experiments reported here tested the possibility that increased mineralocorticoids change the number and/or affinity of Ang receptors in the brain. Rats were given a series of deoxycorticosterone acetate (DOCA) injections (500 micrograms/day, s.c., for 4 days) which are known to produce a salt appetite when given in conjunction with an intracerebroventricular injection of Ang. The binding of 125I-Ang II to membranes prepared from the septal-anteroventral third ventricular region was then examined. DOCA treatment resulted in a significant increase in the number of Ang binding sites (Bmax) with no change in binding affinity (Kd). The binding of 125I-Ang II was then investigated in membranes prepared from 12 other brain regions as well as the pituitary and adrenal gland, showing that the increase in binding capacity occurred in only a few specific brain regions. A third experiment verified that the DOCA treatment used here was sufficient to arouse a salt appetite when combined with a single intracerebroventricular injection of Ang II. The mechanism that underlies the production of salt appetite by aldosterone and Ang II may at least partially consist of mineralocorticoid-induced increases in the number of Ang receptors in discrete brain regions.