The influence exerted by somatostatin on the secretion of ACTH and opioid peptides has still to be clarified. To gain further information on this issue, we performed in 10 normal volunteers two CRF tests (100 ug i.v.) one of which was preceded by s.c. injection of 100 ug of the long-acting somatostatin analogue SMS 201-995 (Sandostatin, Sandoz) (SMS), given 30 minutes before CRF. Premedication with SMS markedly inhibited the response of β-EP to CRF, leaving unchanged the response of β-LPH, ACTH and cortisol: mean incremental areas of β-EP were 199.8 ± 49.31 (SEM) vs 532.9 ± 95.91 pmol/120 min (P <0.01) in the CRF test with and without SMS, respectively. To interpret the selective inhibitory effect of SMS on CRF-stimulated β-EP secretion, it can be hypothesized that: a) the action of SMS was confined to a population of pituicytes preferentially secreting β-EP; b) SMS interfered with the processing of POMC inhibiting the formation of β-EP; c) SMS acted on extrapituitary, possibly peripheral, sources of β-EP. In conclusion, this study indicates that, in man, somatostatin selectively inhibits the CRF-induced secretion of β-EP, but not that of ACTH and β-LPH, by an action that may be exerted at pituitary or extrapituitary level. This is a further example of dissociated secretion of POMC-derived peptides.
|Number of pages||3|
|Journal||Hormone and Metabolic Research|
|Publication status||Published - 1991|
- Corticotropin Releasing Factor
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