DIFFERENT EFFECTS OF DELTA-SLEEP-INDUCING PEPTIDE ON ARGININE-VASOPRESSIN AND ACTH-SECRETION IN NORMAL MEN

Delta-sleep-inducing peptide (DSIP) is a well-known inhibitor of pitui tary ACTH secretion. In order to evaluate the possible influence of DS IP on basal arginine-vasopressin (AVP) secretion and/or on the AVP-res ponse to osmotic and pressure/volumetric stimuli, DSIP (25 nmol/kg) wa s infused in 10 min to 8 normal men (23-34 years old) just before a 2- hour influsion of normal saline (NaCl 0.9%; DSIP test) or hypertonic s aline (0.51 M NaCl; osmotic test) or before an orthostatic test (stand ing upright and maintaining an orthostatic position for 20 min). In di fferent occasions, a 10-min infusion of normal saline (placebo) was gi ven instead of DSIP. In an additional 7 subjects, DSIP or placebo was given 60 min before hypertonic saline or the orthostatic test. The res ults obtained after the administration of DSIP at time 0 and at -60 mi n were similar. Results: The administration of DSIP or normal saline a lone did not change the concentrations of circulating AVP. A slight ph ysiological decline in ACTH levels was observed during saline infusion , whereas a significant decrease in ACTH levels was induced by DSIP ad ministration. Osmotic stimulation of AVP secretion by hypertonic NaCl induced a significant increase in plasma AVP concentrations which was not modified by DSIP administration. The ACTH secretory patterns durin g hypertonic NaCl and hypertonic NaC1 plus DSIP were similar to those observed during normal saline and normal saline plus DSIP, respectivel y. The orthostatic test provided similar plasma AVP increments, regard less of the previous treatment with DSIP. These data show that in cont rast with the inhibitory effects on ACTH, DSIP is not involved in the control of AVP secretion in basal conditions and after osmotic or pres sure/volumetric stimulation. Furthermore, the observation that the inh ibitory effects of DSIP on ACTH secretion were similar during normal a nd hypertonic saline infusions, regardless of osmotically stimulated A VP secretion, argues against a role of AVP in the regulation of the in hibitory action of DSIP on ACTH secretion. Finally, since the rise of endogenous AVP in response to a hypertonic stimulus was unable to stim ulate ACTH secretion and to counteract DSIP inhibitory effect on ACTH, AVP does not appear to be a secretagogue of ACTH in these experimenta l conditions.