Somatostatin acts via a pertussis toxin-sensitive mechanism on calcitonin secretion in C-cells.

The effect of the somatostatin analog octreotide on cAMP-mediated calcitonin (CT) secretion and cAMP accumulation in C-cells was investigated. Glucagon stimulated cAMP accumulation and CT secretion with a maximal effect at a concentration of 10(-6) M. The cAMP antagonist RpcAMPs blocked the glucagon-induced CT secretion down to control levels. Therefore, no other second messengers seem to be involved in glucagon-stimulated CT secretion. Octreotide in increasing doses (10(-9) to 10(-6) M) inhibited cAMP accumulation and CT secretion with a maximal effect at a concentration of 10(-7) (40% and 29% of control values, respectively). Pretreatment of the cells with 100 ng/mL pertussis toxin for 24 hours abolished the inhibitory effect of octreotide on cAMP accumulation and CT secretion (82% and 58% of control values, respectively). Similar results were obtained under the influence of the phosphodiesterase inhibitor IBMX. Therefore, we conclude that somatostatin modulates adenylate cyclase-coupled CT secretion in C-cells via a pertussis toxin-sensitive G-protein possibly in an autocrine/paracrine way.