Brain vasopressin and sodium appetite.
Intraventricular injections of vasopressin (VP) and antagonists with varying degrees of specificity for the VP receptors were used to identify the action of endogenous brain VP on 0.3 M NaCl intake by sodium-deficient rats. Lateral ventricular injections of 100 ng and 1 microg VP caused barrel rotations and a dramatic decrease in NaCl intake by sodium-deficient rats and suppressed sucrose intake. Intraventricular injection of the V(1)/V(2) receptor antagonist [d(CH(2))(5)(1),O-Et-Tyr(2),Val(4), Arg(8)]VP and the V(1) receptor antagonist [d(CH(2))(5)(1),O-Me-Tyr(2),Arg(8)]VP (MeT-AVP) significantly suppressed NaCl intake by sodium-deficient rats without causing motor disturbances. MeT-AVP had no effect on sucrose intake (0.1 M). In contrast, the selective V(2) receptor antagonist had no significant effect on NaCl intake. Last, injections of 100 ng MeT-AVP decreased mean arterial blood pressure (MAP), whereas 100 ng VP elevated MAP and pretreatment with MeT-AVP blocked the pressor effect of VP. These results indicate that the effects produced by 100 ng MeT-AVP represent receptor antagonistic activity. These findings suggest that the effect of exogenous VP on salt intake is secondary to motor disruptions and that endogenous brain VP neurotransmission acting at V(1) receptors plays a role in the arousal of salt appetite.[1]References
- Brain vasopressin and sodium appetite. Flynn, F.W., Kirchner, T.R., Clinton, M.E. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2002) [Pubmed]
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