Sodium (Na+) depletion induces sodium appetite to replenish Na+ loss.
It appears to be a consequence of enhanced levels of aldosterone (Aldo
) and angiotensin II (AII) in the plasma as well as in the brain. Mine
ralocorticoid pretreatment modifies the sensitivity of septo-preoptic
neurons to locally applied An and Aldo. Therefore, we investigated sep
to-preoptic neuronal sensitivities to AII and Aldo, as well as to the
specific AII type-1 receptor (AT-1) non-peptide antagonist losartan (L
os) and to the specific AII type-2 receptor (AT-2) non-peptide antagon
ist PD123319 after one Na+ depletion without repletion. We found that
one Na+ depletion induced increases in the proportion of neurons inhib
ited by iontophoretic application of ALI (20.5% vs. 7.8%, p=0.004) whe
reas, the proportion of neurons excited by Aldo was increased, (23.7%
vs. 5%, p=0.001). Moreover, the proportion of neurons changing sensiti
vity to AII after one application of Aldo was increased in the furosem
ide group (44.2% vs. 20.4%, p=0.0123). The proportion of neurons inhib
ited by application of losartan was enhanced, (26.4% vs. 9.3%, p=0.03)
. No significant changes were found in response to PD123319 by itself.
Moreover, there were more neurons which co-localized responses to bot
h Los and PD123319 in the furosemide group than in the control group (
29.7% vs. 8.6%, p=0.027). It is known that multidepletions induce an i
ncreased need-free sodium appetite and our present findings could well
form part of the neuronal basis of this behavior. (C) 1998 Elsevier S
cience B.V.