EFFECTS OF OVINE CORTICOTROPIN-RELEASING HORMONE INJECTION AND DESMOPRESSIN COADMINISTRATION ON GALANIN AND ADRENOCORTICOTROPIN PLASMA-LEVELS IN NORMAL WOMEN

The neuropeptide galanin (GAL) has been shown to be located in the pit uitary gland and to modulate the secretion of several pituitary hormon es. In the human pituitary, GAL is almost exclusively located within c orticotrophs. We examined whether GAL is secreted from corticotrophs i n response to stimuli that induce ACTH release. Plasma levels of GAL a nd ACTH were evaluated in six healthy female subjects in the follicula r phase of the menstrual cycle after the following treatments: 1) ovin e CRH (oCRH) injection during saline (SAL) infusion, 2) oCRH injection during infusion of the arginine vasopressin analog desmopressin (DP), 3) SAL injection during DP infusion, and 4) SAL injection during SAL infusion. DP (4.3 ng/min kg BW) or SAL was infused from 0-60 min. oCRH (1 mu g/kg BW) or SAL was administered by a 2-min injection at 5 min. The expected ACTH response to oCRH was enhanced by the concomitant DP administration (peak level, 10.39 +/- 1.12 us. 21.37 +/- 3.43 pmol/L i n SAL infusion plus oCRH injection vs. DP infusion plus oCRH injection , respectively; P < 0.05). The mean integrated ACTH response, expresse d as the area under the curve, to SAL infusion plus oCRH injection vs. that to DP infusion plus oCRH injection was 288.23 +/- 61.94 vs. 699. 70 +/- 91.80 pmol/L 60 min, respectively (P < 0.05). A slight, but not significant, increase was observed in ACTH values after DP infusion p lus SAL injection compared to that after SAL infusion plus SAL injecti on challenge. Plasma GAL levels were highly variable. No changes in GA L levels were found concomitant to ACTH values in either experimental group. In fact, GAL levels were not significantly affected by either t reatment. These data confirm that DP potentiates the ACTH response to CRH in humans. Furthermore, our results suggest that GAL is probably n ot cosecreted With ACTH in normal subjects. The possibility exists tha t GAL produced by corticotrophs exerts its action principally through a locally mediated paracrine or autocrine mechanism without being secr eted into the bloodstream.