title: A central Na+ receptor and its influence on osmotic and angiotensin II induced drinking in the pigeon Columbia livia.
abstract: Drinking in response to peripheral osmotic stimuli has been shown to be initiated via an osmoreceptor mechanism. Andersson and his colleagues, from work in the goat, have challenged this hypothesis. They have found that the CSF concentration of Na is the most important factor and that an increase causes thirst, ADH release, and a decrease in Na sodium appetite. We have investigated this subject using pigeons since they have large cerebroventricular spaces and are very rapid drinkers. Pigeons were found to respond normally to peripheral osmotic stimuli but only hypertonic NaCl centrally. Central infusions of water inhibited drinking in response to simultaneous i.v. infusions of 0.5 M NaCl or 1.0 M sucrose. The inhibition occurred only during the infusion and drinking recovered rapidly to normal shortly afterwards. Hypertonic sucrose (0.9 M) centrally inhibited drinking to the same peripheral stimuli whereas 0.3 M sucrose centrally blocked drinking only during i.v. infusion of 0.5 M NaCl but not i.v. 1.0 M sucrose. Drinking recovered rapidly after the infusion. Hypertonic NaCl centrally potentiated drinking to peripheral osmotic stimuli. Urine and electrolyte excretion was increased after hypertonic sucrose infused simultaneously i.c.v. and i.v. compared with other solutions infused i.c.v. and hypertonic sucrose i.v. Drinking induced by AII centrally was additive with hypertonic NaCl centrally. AII infused centrally in water halved the drinking response. AII infused peripherally was not affected by central decreases in Na but additive with increases. Thus there appears to be a central receptor mechanism for Na but it seems to act as a "permissive gate", rather than a potentiator, regulating drinking in response to peripheral or central osmotic stimuli or AII.
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001769:Blood; D010856:Columbidae / Q000502:physiology*; D004231:Diuresis / Q000187:drug effects; D004326:Drinking / Q000187:drug effects*; D005947:Glucose / Q000494:pharmacology; D008353:Mannitol / Q000494:pharmacology; D009994:Osmolar Concentration; D012964:Sodium / Q000097:blood / Q000134:cerebrospinal fluid / Q000378:metabolism / Q000502:physiology*; D012965:Sodium Chloride / Q000494:pharmacology; D012996:Solutions; D013395:Sucrose / Q000494:pharmacology; D014508:Urea / Q000494:pharmacology; D014556:Urine; D014882:Water-Electrolyte Balance
chemical_list: D012996:Solutions; D000804:Angiotensin II; D008353:Mannitol; D012965:Sodium Chloride; D013395:Sucrose; D014508:Urea; D012964:Sodium; D005947:Glucose