Effect of Sandostatin on CRF-Stimulated Secretion of ACTH, β-Lipotropin and β-Endorphin

Summary

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 βEP to CRF, leaving unchanged the response of βLPH, ACTH and cortisol: mean incremental areas of βEP 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 βEP secretion, it can be hypothesized that: a) the action of SMS was confined to a population of pituicytes preferentially secreting βEP; b) SMS interfered with the processing of POMC inhibiting the formation of βEP; c) SMS acted on extrapituitary, possibly peripheral, sources of βEP.

In conclusion, this study indicates that, in man, somatostatin selectively inhibits the CRF-induced secretion of βEP, but not that of ACTH and βLPH, by an action that may be exerted at pituitary or extrapituitary level. This is a further example of dissociated secretion of POMC-derived peptides.

Key words

Somatostatin - β-Endorphin - Corticotropin Releasing Factor