Alpha-adrenergic agonists inhibit the dipsogenic effect of angiotensin II by their stimulation of atrial natriuretic peptide release

• Published in: Brain research Vol. 895; no. 1; pp. 80 - 88
• Main Authors: Bastos, Rosemary, Favaretto, Ana Lúcia Vianna, Gutkowska, Jolanta, McCann, Samuel M, Antunes-Rodrigues, José
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 23-03-2001; Amsterdam Elsevier; New York, NY
• Subjects: Adrenergic alpha-Agonists - pharmacology; Angiotensin II - antagonists & inhibitors; Angiotensin II - metabolism; Angiotensin II - pharmacology; Animals; Atrial Natriuretic Factor - blood; Atrial Natriuretic Factor - drug effects; AV3V; Biological and medical sciences; Clonidine (α 2-adrenergic agonist); Clonidine - pharmacology; Dose-Response Relationship, Drug; Drinking - drug effects; Drinking - physiology; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; Hypothalamus - drug effects; Hypothalamus - metabolism; Injections, Intraventricular; Male; median eminence; Neurons - drug effects; Neurons - metabolism; Phenylephrine (α 1-adrenergic receptor agonist); Phenylephrine - pharmacology; Plasma ANP; Rats; Rats, Wistar; Sodium Chloride - pharmacology; Vertebrates: anatomy and physiology, studies on body, several organs or systems; Water intake; Water-Electrolyte Balance - drug effects; Water-Electrolyte Balance - physiology; Endocrine and autonomic regulation; Phenylephrine (α 1-adrenergic receptor agonist); Water intake; Plasma ANP; Clonidine (α 2-adrenergic agonist); AV3V; Agonist; Rat; Rodentia; Drinking; Atrial natriuretic peptide; Renin angiotensin system; Vertebrata; Natriuretic hormone; Mammalia; α-Adrenergic receptor; Angiotensin II; Release
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(01)02033-9

Angiotensin II (ANG-II) and atrial natriuretic peptide (ANP) have opposing actions on water and salt intake and excretion. Within the brain ANP inhibits drinking induced by ANG-II and blocks dehydration-induced drinking known to be caused by release of ANG-II. Alpha-adrenergic agonists are known to release ANP and antagonize ANG II-induced drinking. We examined the hypothesis that α agonists block ANG-II-induced drinking by stimulating the release of ANP from ANP-secreting neurons (ANPergic neurons) within the brain that inhibit the effector neurons stimulated by ANG-II to induce drinking. Injection of ANG-II (12.5 ng) into the anteroventral region of the third ventricle (AV3V) at the effective dose to increase water intake increased plasma ANP concentrations (
P<0.01) within 5 min. As described before, previous injection of phenylephrine (an α
1-adrenergic agonist) or clonidine (an α
2-adrenergic agonist) into the AV3V region significantly reduced ANG-II-induced water intake. Their injection also induced a significant increase in plasma ANP concentration and in ANP content in the olfactory bulb (OB), AV3V, medial basal hypothalamus (MBH) and median eminence (ME). These results suggest that the inhibitory effect of both α-adrenergic agonists on ANG-II-induced water intake can be explained, at least in part, by the increase in ANP content and presumed release from these neural structures. The increased release of ANP from the axons of neurons terminating on the effector neurons of the drinking response by stimulation of ANP receptors would inhibit the stimulatory response evoked by the action of ANG-II on its receptors on these same effector neurons.