Arginine vasopressin and adrenocorticotropin secretion in response to psychosocial stress is attenuated by ethanol in sons of alcohol-dependent fathers

Abstract

Familial risk and environmental stress promote the development of alcohol dependence. We investigated whether a positive family history of alcoholism affects the neuroendocrine response to a standardized laboratory stress test in healthy subjects without alcohol use disorders. Twenty-four high-risk subjects with a paternal history of alcoholism (PHA) and 16 family history negative (FHN) controls were evaluated. Psychosocial stress was induced by having subjects deliver a 5-min speech and mental arithmetics in front of an audience on separate days, after drinking either placebo or ethanol (0.6 g/kg) in a randomized sequence. Adrenocorticotropin (ACTH) was measured in 10 plasma samples covering up to 75 min after the stress test. Plasma arginine vasopressin (AVP) was determined before the stressor, at the time of maximum ACTH secretion, and at 75 min after stress onset. The stress test induced a phasic increase in ACTH secretion. At the time of maximum ACTH, AVP was significantly increased in relation to baseline. Compared to placebo, alcohol administration significantly attenuated maximum ACTH concentration in PHA but not FHN subjects, and decreased AVP measured in the same samples in PHA but not FHN subjects. We conclude that activation of the hypothalamic-pituitary-adrenal system by psychosocial stress is accompanied by an increase in peripheral plasma AVP levels. Secretion of both ACTH and AVP suggest that alcohol attenuates the stress response selectively in PHA but not FHN subjects. This might imply some short-term positive alcohol effect in sons of alcoholics, but also constitute a mechanism by which their risk to develop alcohol use disorders is increased.

The Limbic-Hypothalamic-Pituitary-Adrenal Axis and the Development of Alcohol Use Disorders in Youth

“…In others, however, both performance stressors and dosing of opioid antagonists are associated with exaggerated cortisol responses in those with a family history (Uhart et al, 2006; Wand et al, 1998; Zimmermann et al, 2004a). This effect may be attenuated after alcohol consumption (Zimmermann et al, 2004b). …”

Support for two increased vasopressinergic activities in depression at large and the differential effect of antidepressant treatment

“…However, because the amount of AVP released by these neurons into the bloodstream is probably too small to be detected in peripheral plasma, and no stress-related increase of plasma AVP or AVP-cortisol correlation has been found in the male rat model of chronic stress and depression (Aguilera et al, 2008), nor in the stressed male HAB rat (Landgraf et al, 1999), these male rat models are not useful to test the hypothesis of increased V1b receptor function in depression as the cause of the correlating peripheral AVP and cortisol concentrations in human depression. As this correlation is not due to osmotic stimulation of AVP release, because plasma AVP in depression has previously been found to have no correlation with plasma osmolality (Brunner et al, 2002;Van Londen et al, 1997), the most appropriate animal model of depression should show a non-osmotic stress-related AVP response, as has been found in acutely stressed healthy human subjects (Zimmermann et al, 2004) and in chronically depressed patients (Van Londen, 2003). We therefore suggest that tests of the hypothesis of increased AVP release and V1b receptor function in depression could better be carried out in female rat models, which in contrast to male rats do have a non-osmotic stress-induced plasma AVP response (Williams et al, 1985).…”

Transient Inactivation of Shell Part of Nucleus Accumbens Inhibits and Exacerbates Stress-Induced Metabolic Alterations in Wistar Rats

“…This result is in agreement with those of previous studies (Sarahian et al, 2015). It is postulated that the vasopressin hormone released during stress from magnocellular cells located in the paraventricular nucleus is responsible for excessive water intake (Zimmermann et al, 2004). In our experiments, transient inactivation of the right side of the NAc shell inhibited the stress effect on water intake, whereas transient inactivation of the left side exacerbated the effect.…”