A novelty-related sustained elevation of vasopressin plasma levels in young men is not associated with an enhanced response of adrenocorticotropic hormone (ACTH) to human corticotropin releasing factor (hCRF).

A comparative study of the effects of intravenously administered corticotropin releasing factor (i.e. exogenous CRF), in the absence or presence of simultaneous opioid receptor blockade, versus stress (i.e. endogenous CRF) on plasma adrenocorticotropic hormone (ACTH), cortisol and vasopressin (AVP) was carried out in ten healthy men (mean age 35.6 +/- 9.5 years) using an intra-individual repeat setting. Three different stimuli were applied blindly and in random order, one per day, in a 3-day experimental block: (1) human (h) CRF; (2) hCRF/naloxone; and (3) a combined multifaceted 5-min stress test. A second block, following the same protocol, was carried out 12 weeks later. Each experimental day lasted from 0700 to 1500 hours, with subjects remaining supine throughout. ACTH and cortisol levels each responded with significant peaks to all three stimulating conditions in both blocks while AVP levels remained unaffected by any of these stimuli. Unexpectedly, in five of the ten subjects significantly elevated AVP basal concentrations were measured throughout the first block. This phenomenon appeared to be age-related, being observed in younger men only (29.6 +/- 5.2 vs 41.6 +/- 9.2 years; p = 0.03) and was not paralleled by changes in plasma osmolality or blood pressure. In the second block, AVP levels were low and no longer different between younger and older subjects. ACTH and cortisol curves did not differ among subgroups nor between blocks. In conclusion, plasma AVP, in contrast to ACTH, is not acutely influenced by either endogenous or exogenous CRF. However, anticipation of novelty seems to be a human-specific, stress-related stimulus for a sustained elevation of plasma AVP in young men. This novelty-related continuous elevation of AVP levels reported here neither affected basal plasma ACTH nor acted synergistically with exogenous hCRF to increase circulating ACTH.