The mechanism of anticonvulsant-associate hyponatremia has generally been considered to be inappropriate hypersecretion of AVP (Ashton et al., 1977; Smith et al., 1977), but an experimental study has indicated a direct effect of carbamazepine on the kidney through V2R stimulation without evidence of increased release of endogenous AVP (Meinders et al., 1975). Here, AVP is linked to Hyponatremia.