On the mode of action of the pentagastrin test in the carcinoid syndrome.

Abstract

Provocation with pentagastrin (PG) (0.6 micrograms/kg intravenously) causes a release of serotonin (5-hydroxytryptamine (5-HT] in excess of the metabolizing capacity associated with carcinoid symptoms and a moderate fall in systemic arterial blood pressure in patients with midgut carcinoids and hepatic metastases. In this study PG also caused a release of 5-HT into portal circulation of anesthetized cats with stable peripheral levels of 5-HT in whole blood, indicating an effective hepatic metabolization. A similar response was obtained in the same animal when the PG test was repeated after 3 h. PG provocation was also performed in animals before and after adrenalectomy. Adrenalectomy seems to prevent the PG-induced release of 5-HT into portal circulation, indicating involvement of an adrenal mechanism. PG does not induce 5-HT release from cell suspensions of midgut carcinoid tumors, but such release was induced by incubation with adrenoceptor agonists. These findings indicate the presence of adrenoceptors on carcinoid tumor cells. The mode of action of the PG test may therefore be activation of such adrenoceptors by catecholamines, released from the adrenal medulla at the fall of arterial blood pressure at PG provocation.