Central α2-adrenoceptors and the pontine lateral parabrachial nucleus
(LPBN) are involved in the control of sodium and water intake. Bilateral injections
of moxonidine (α2-adrenergic/imidazoline receptor agonist) or
noradrenaline into the LPBN strongly increases 0.3 M NaCl intake induced by a
combined treatment of furosemide plus captopril. Injection of moxonidine into the
LPBN also increases hypertonic NaCl and water intake and reduces oxytocin secretion,
urinary sodium, and water excreted by cell-dehydrated rats, causing a positive sodium
and water balance, which suggests that moxonidine injected into the LPBN deactivates
mechanisms that restrain body fluid volume expansion. Pretreatment with specific
α2-adrenoceptor antagonists injected into the LPBN abolishes the
behavioral and renal effects of moxonidine or noradrenaline injected into the same
area, suggesting that these effects depend on activation of LPBN
α2-adrenoceptors. In fluid-depleted rats, the palatability of sodium is
reduced by ingestion of hypertonic NaCl, limiting intake. However, in rats treated
with moxonidine injected into the LPBN, the NaCl palatability remains high, even
after ingestion of significant amounts of 0.3 M NaCl. The changes in behavioral and
renal responses produced by activation of α2-adrenoceptors in the LPBN are
probably a consequence of reduction of oxytocin secretion and blockade of inhibitory
signals that affect sodium palatability. In this review, a model is proposed to show
how activation of α2-adrenoceptors in the LPBN may affect palatability
and, consequently, ingestion of sodium as well as renal sodium excretion.