Multifactorial control of water and saline intake: role of <FONT FACE=Symbol>a</font>2-adrenoceptors

Abstract

Water and saline intake is controlled by several mechanisms activated during dehydration. Some mechanisms, such as the production of angiotensin II and unloading of cardiovascular receptors, activate both behaviors, while others, such as the increase in blood osmolality or sodium concentration, activate water, but inhibit saline intake. Aldosterone probably activates only saline intake. Clonidine, an α 2 -adrenergic agonist, inhibits water and saline intake induced by these mechanisms. One model to describe the interactions between these multiple mechanisms is a wire-block diagram, where the brain circuit that controls each intake is represented by a summing point of its respective inhibiting and activating factors. The α 2 -adrenoceptors constitute an inhibitory factor common to both summing points.

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

“…Bilateral injections of RX 821002 into the LPBN abolished the effects of noradrenaline and α-methylnoradrenaline in the same area on 0.3 M NaCl (2,39). The increase in sodium intake after LPBN moxonidine or noradrenaline injection in fluid-depleted rats (2,38,39) sharply contrasts with the inhibitory effect that α 2 -adrenoceptor activation in the forebrain has on sodium appetite and thirst (1,9,11-13). Therefore, forebrain and hindbrain (or more specifically LPBN) α 2 -adrenergic mechanisms play opposite roles in water and sodium intake (38,39).…”

“…Its effects depend on the area of the encephalon studied, the type of treatment the animal receives, and the receptors involved (for a review see Refs. 1,2). Early studies using mixed α 2 -adrenergic and imidazoline receptor agonists, like clonidine and moxonidine, injected into the lateral and third cerebral ventricles, septal area, lateral preoptic area, and lateral hypothalamus showed that they are effective in inhibiting water and sodium intake induced by different stimuli (1,3-10).…”

“…Early studies using mixed α 2 -adrenergic and imidazoline receptor agonists, like clonidine and moxonidine, injected into the lateral and third cerebral ventricles, septal area, lateral preoptic area, and lateral hypothalamus showed that they are effective in inhibiting water and sodium intake induced by different stimuli (1,3-10). The inhibition of either water or hypertonic NaCl intake with forebrain injections of moxonidine or clonidine was reduced by pretreatment with injections of α 2 -adrenoceptor antagonists, like yohimbine or RX 821002 (1,9,11-13). Norepinephrine, the endogenous ligand with no imidazoline characteristics, injected intracerebroventricularly ( icv ), also inhibits water and NaCl intake, an effect antagonized by pretreatment with idazoxan, an α 2 -adrenergic and imidazoline receptor antagonist (1).…”

“…The inhibition of either water or hypertonic NaCl intake with forebrain injections of moxonidine or clonidine was reduced by pretreatment with injections of α 2 -adrenoceptor antagonists, like yohimbine or RX 821002 (1,9,11-13). Norepinephrine, the endogenous ligand with no imidazoline characteristics, injected intracerebroventricularly ( icv ), also inhibits water and NaCl intake, an effect antagonized by pretreatment with idazoxan, an α 2 -adrenergic and imidazoline receptor antagonist (1). These results suggest that α 2 -adrenoceptor activation in the forebrain inhibits water and NaCl intake.…”