Delta-sleep-inducing peptide (DSIP) is a well-known inhibitor of pituitary ACTH secretion. In order to evaluate the possible influence of DSIP on basal arginine-vasopressin (AVP) secretion and/or on the AVP-response to osmotic and pressure/volumetric stimuli, DSIP (25 nmol/kg) was 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 saline (0.51 M NaCl; osmotic test) or before an orthostatic test (standing upright and maintaining an orthostatic position for 20 min). In different occasions, a 10-min infusion of normal saline (placebo) was given instead of DSIP. In an additional 7 subjects, DSIP or placebo was given 60 min before hypertonic saline or the orthostatic test. The results obtained after the administration of DSIP at time 0 and at -60 min were similar. Results: The administration of DSIP or normal saline alone did not change the concentrations of circulating AVP. A slight physiological decline in ACTH levels was observed during saline infusion, whereas a significant decrease in ACTH levels was induced by DSIP administration. 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 during hypertonic NaCl and hypertonic NaCl plus DSIP were similar to those observed during normal saline and normal saline plus DSIP, respectively. The orthostatic test provided similar plasma AVP increments, regardless of the previous treatment with DSIP. These data show that in contrast with the inhibitory effects on ACTH, DSIP is not involved in the control of AVP secretion in basal conditions and after osmotic or pressure/volumetric stimulation. Furthermore, the observation that the inhibitory effects of DSIP on ACTH secretion were similar during normal and hypertonic saline infusions, regardless of osmotically stimulated AVP secretion, argues against a role of AVP in the regulation of the inhibitory action of DSIP on ACTH secretion. Finally, since the rise of endogenous AVP in response to a hypertonic stimulus was unable to stimulate ACTH secretion and to counteract DSIP inhibitory effect on ACTH, AVP does not appear to be a secretagogue of ACTH in these experimental conditions.

Keywords:
Delta-sleep-inducing peptide, Arginine-vasopressin, ACTH, Hypovolemia, Hypertonic saline
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© 1994 S. Karger AG, Basel
1994
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