Animal models of depression support a pathogenetic role for vasopressinergic activation involving increased arginine vasopressin (AVP) release and AVP receptor (V1b) synthesis. Evidence of this has been found particularly in patients with highly anxious-retarded (HAR) and above-normal AVP (ANA) depression. A general pathogenetic theory however predicts vasopressinergic activities to play a role in at least all major depressive disorders, and antidepressant (AD) treatment to be mediated by vasopressinergic reduction. We tested these hypotheses by re-analysing the data of 66 depressed patients; 27 with and 39 without AD treatment. The plasma AVP concentration and the AVP-cortisol correlation were used as presumed parameters of AVP release and pituitary V1b receptor function. A high AVP-cortisol correlation (r = 0.72; p < 0.001) was found in the non-AD group, and no correlation in the AD treatment group. AD treatment did not relate to plasma AVP concentration. The AVP-cortisol correlation in HAR and ANA depression was not explained by a low rate of AD treatment. These human data support the hypothesis of increased AVP release and receptor function as pathogenetic characteristics of major depression, and show selective normalization of the AVP-cortisol correlation, which is supposed to reflect the receptor function, by AD treatment.
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