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

Abstract

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.

Gabaergic and opioid receptors mediate the facilitation of NaCl intake induced by α2-adrenergic activation in the lateral parabrachial nucleus

“…In conclusion, the present and previous studies [19,34,35,38] suggest that moxonidine acting in ␣ 2 -adrenoceptors in the LPBN increases the release of GABA and opioids and blocks serotonin action, reducing the activity of the inhibitory mechanisms, which might enhance ingestive reactions and reduces rejection responses caused by the ingestion of 0.3 M NaCl and water, increasing the intake.…”

Neurochemistry of the Kölliker‐Fuse nucleus from a respiratory perspective

“…A wide range of histological methods, including autoradiography and in situ hybridization, indicate the presence of α2 receptors in the pontine nuclei, including the parabrachial nuclei and the KF (Andrade, Andrade‐Franzé, Paula, De, & De, 2014; Davern, 2014; Herbert & Flügge, 1995; Scheinin et al., 1994; Unnerstall, Fernandez, & Orensanz, 1985). Specifically, moderate to intense labeling for α2A and α2B‐receptor subtypes has been documented in the KF of multiple species (Rosin et al., 1993; Strazielle, Lalonde, Hébert, & Reader, 1999; Tavares, Handy, Bogdanova, Rosene, & Gavras, 1996; Wang et al., 1996).…”

Rapid stimulation of sodium intake combining aldosterone into the 4th ventricle and the blockade of the lateral parabrachial nucleus

“…Aldosterone into the 4th V also produces no change in arterial pressure, which excludes the involvement of cardiovascular signals in the natriorexigenic response to aldosterone into the 4th V. On the hand, previous studies showed that the deactivation of the LPBN mechanisms with injections of moxonidine or methysergide into the LPBN reduced renal excretion of sodium and water, which suggests that LPBN mechanisms act facilitating renal excretion (Margatho et al, 2007;Andrade et al, 2012). Therefore, previous results suggest that LPBN mechanisms reducing sodium ingestion and increasing the excretion prevent the expansion of body fluid volume (Andrade et al, 2014. The present results suggest for the first time that the natriorexigenic signals produced by aldosterone acting in the hindbrain are also inhibited by LPBN mechanisms.…”