Acute sodium depletion modifies septo-preoptic neuron sensitivities to neurohormones.

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. Mineralocorticoid pretreatment modifies the sensitivity of septo-preoptic neurons to locally applied AII and Aldo. Therefore, we investigated septo-preoptic neuronal sensitivities to AII and Aldo, as well as to the specific AII type-1 receptor (AT-1) non-peptide antagonist losartan (Los) and to the specific AII type-2 receptor (AT-2) non-peptide antagonist PD123319 after one Na+ depletion without repletion. We found that one Na+ depletion induced increases in the proportion of neurons inhibited by iontophoretic application of AII (20.5% vs. 7.8%, p=0.004) whereas, the proportion of neurons excited by Aldo was increased, (23.7% vs. 5%, p=0.001). Moreover, the proportion of neurons changing sensitivity to AII after one application of Aldo was increased in the furosemide group (44.2% vs. 20.4%, p=0.0123). The proportion of neurons inhibited 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 both 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 increased need-free sodium appetite and our present findings could well form part of the neuronal basis of this behavior.