Ma. Sato et al., IDAZOXAN AND THE EFFECT OF INTRACEREBROVENTRICULAR OXYTOCIN OR VASOPRESSIN ON SODIUM-INTAKE OF SODIUM-DEPLETED RATS, Regulatory peptides, 69(3), 1997, pp. 137-142
The alpha(2)-adrenergic agonist clonidine and the neuropeptide oxytoci
n, inhibit sodium intake when injected intracerebroventricularly (i.c.
v.). The present work investigates whether (1) vasopressin also inhibi
ts sodium intake when injected i.c.v., and (2) the effect of oxytocin
and of vasopressin on sodium intake is affected by i.c.v. injection of
idazoxan, an alpha(2)-adrenergic antagonist. Clonidine (30 nmol), oxy
tocin (40, 80 nmol) and vasopressin (40, 80 nmol) were injected i.c.v.
20 min prior to a 1.5% NaCl appetite test, in rats depleted of sodium
for 24 h by a combination of a single s.c. injection of furosemide (1
0 mg/rat) and removal of ambient sodium. Every dose of clonidine, oxyt
ocin and vasopressin inhibited the 1.5% NaCl intake. Seizures were obs
erved with the higher dose of vasopressin, but not with either dose of
oxytocin. The effect of i.c.v. injection of clonidine (30 nmol), oxyt
ocin (80 nmol) or vasopressin (40 nmol) was partially inhibited by pri
or i.c.v. injection of idazoxan (160, 320 nmol). The results suggest t
hat the inhibition of 1.5% NaCl intake induced by i.c.v. injection of
neuropeptides in sodium-depleted rats depends, in part, on the activat
ion of central alpha(2)-adrenoceptors. (C) 1997 Elsevier Science B.V.
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