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Am J Physiol Regul Integr Comp Physiol 282: R1236-R1244, 2002; doi:10.1152/ajpregu.00181.2001
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Vol. 282, Issue 4, R1236-R1244, April 2002

Brain vasopressin and sodium appetite

Francis W. Flynn, Thomas R. Kirchner, and Margaret E. Clinton

Department of Zoology and Physiology and Neuroscience Program, University of Wyoming, Laramie, Wyoming 82071

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 µg VP caused barrel rotations and a dramatic decrease in NaCl intake by sodium-deficient rats and suppressed sucrose intake. Intraventricular injection of the V1/V2 receptor antagonist [d(CH2)51,O-Et-Tyr2,Val4, Arg8]VP and the V1 receptor antagonist [d(CH2)51,O-Me-Tyr2,Arg8]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 V2 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 V1 receptors plays a role in the arousal of salt appetite.

neurohypophysial peptides; taste; blood pressure; V1 receptor; V2 receptor


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