Deuterium induced extinction of ADH-release in response to intracerebroventricular infusions of hypertonic NaCl and angiotensin.
Infusions (20 microliter/min) of hypertonic (0.3 M) NaCl and angiotensin II (1 ng/kg min-1) in isotonic (0.15 M) NaCl were made for 1 h in the hydrated goat during fully developed water diruesis. Either H2O or deuterium (D2O) WAS USED AS SOLVENT. A pronounced antidiuretic response, outlasting the infusion period by 30 min or more, was seen when the substances were dissolved in H2O. Only a weak inhibition of the water diuresis, which was extinguished during the infusion period, was obtained when D2O was used as the solvent. The infusion of 0.3 M NaCl/H2O invariably induced drinking in one of the goats, which, however, showed no drinking response to the infusions of 0.3 M NaCl/D2O. The possibility is discussed that D2O (perhaps by its inhibitory effect on (Na+-K+)-ATPase activity) reduced the sensitivity of juxtaventricular receptors regulating ADH-release and water intake.
D000804:Angiotensin II / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D003903:Deuterium / Q000008:administration & dosage / Q000494:pharmacology*; D004231:Diuresis / Q000187:drug effects; D004326:Drinking / Q000187:drug effects; D005260:Female; D006041:Goats; D007276:Injections, Intraventricular; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage / Q000494:pharmacology*; D012965:Sodium Chloride / Q000494:pharmacology*; D014667:Vasopressins / Q000378:metabolism*; D014867:Water / Q000008:administration & dosage / Q000494:pharmacology
D012462:Saline Solution, Hypertonic; D014867:Water; D014667:Vasopressins; D000804:Angiotensin II; D012965:Sodium Chloride; D003903:Deuterium