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Abstract
The subfornical organ plays a role in a number of the effects of blood-borne angiotensin II (ANG II) including the increase in water drinking and blood pressure and the release of vasopressin from the pituitary. Recently it has been shown that systemically administered ANG II also reduces voluntary alcohol intake. The present study assessed the role of the SFO in alcohol consumption by examining the effects of SFO lesions on voluntary alcohol intake and on the suppression of voluntary alcohol intake by ANG II. Whereas the lesion did not alter alcohol consumption per se, it did significantly attenuate the ability of ANG II to reduce alcohol intake. This effect was not due to a lesion-induced change in the pharmacokinetics of alcohol and was observed only in those animals whose lesions produced a functional deficit, i.e., abolishing the increase in water drinking produced by ANG II. These results indicate that the SFO mediates the effect of systemically administered ANG II on alcohol intake but does not otherwise affect the regulation of alcohol consumption.
Published Version
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