Multifactorial control of water and saline intake: Role of α2-adrenoceptors

• Autor(a) principal: De-Luca, L. A. [UNESP]
• Data de Publicação: 1997
• Outros Autores: Menani, José Vanderlei [UNESP]
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://dx.doi.org/10.1590/S0100-879X1997000400011; http://hdl.handle.net/11449/65080
• topic: α2-Adrenergic agonist; Clonidine; Dehydration; Noradrenaline; Sodium intake; Water intake; alpha 2 adrenergic receptor; alpha adrenergic receptor stimulating agent; clonidine; noradrenalin; sodium chloride; animal; dehydration; drinking; drug effect; metabolism; physiology; renin angiotensin aldosterone system; review; Adrenergic alpha-Agonists; Animals; Drinking; Norepinephrine; Receptors, Adrenergic, alpha-2; Renin-Angiotensin System; Sodium Chloride

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, anα2-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 α2-adrenoceptors constitute an inhibitory factor common to both summing points.