Role of α2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis

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 combin...

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Main Authors: C.A.F. Andrade, G.M.F. Andrade-Franze, P.M. De Paula, L.A. De Luca Jr., J.V. Menani
Format: Article
Language:English
Published: Associação Brasileira de Divulgação Científica 2014-01-01
Series:Brazilian Journal of Medical and Biological Research
Subjects:
Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014000100011&lng=en&tlng=en
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author C.A.F. Andrade
G.M.F. Andrade-Franze
P.M. De Paula
L.A. De Luca Jr.
J.V. Menani
author_facet C.A.F. Andrade
G.M.F. Andrade-Franze
P.M. De Paula
L.A. De Luca Jr.
J.V. Menani
author_sort C.A.F. Andrade
collection DOAJ
description 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.
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spelling doaj.art-e03c3a2a8bc2483ea6f4a462e8d8ba9f2022-12-22T03:55:02ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research1414-431X2014-01-01471111810.1590/1414-431X20133308S0100-879X2014000100011Role of α2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasisC.A.F. AndradeG.M.F. Andrade-FranzeP.M. De PaulaL.A. De Luca Jr.J.V. MenaniCentral 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.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014000100011&lng=en&tlng=enParabrachial nucleusSodiumNatriuresisThirstHindbrainTaste
spellingShingle C.A.F. Andrade
G.M.F. Andrade-Franze
P.M. De Paula
L.A. De Luca Jr.
J.V. Menani
Role of α2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis
Brazilian Journal of Medical and Biological Research
Parabrachial nucleus
Sodium
Natriuresis
Thirst
Hindbrain
Taste
title Role of α2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis
title_full Role of α2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis
title_fullStr Role of α2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis
title_full_unstemmed Role of α2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis
title_short Role of α2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis
title_sort role of α2 adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis
topic Parabrachial nucleus
Sodium
Natriuresis
Thirst
Hindbrain
Taste
url http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014000100011&lng=en&tlng=en
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