INHIBITORY EFFECT OF SOMATOSTATIN ON INSULIN SECRETION DURING α-ADRENERGIC BLOCKADE IN THREE DIFFERENT SPECIES

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Abstract
Somatostatin [S] may suppress insulin release via a stimulation of the inhibitory .alpha.-adrenoceptors of the pancreatic .beta.-cell. The effect of somatostatin on insulin secretion during .alpha.-adrenergic blockade with phentolamine was therefore studied in 3 different species: the rat, the cat and the mouse. S significantly depressed insulin release during .alpha.-adrenoceptor blockade in all 3 species. In the rat, infusion of S at a dose of 0.3 .mu.g/kg per min decreased basal plasma insulin concentration by 92%. In the presence of phentolamine, the same dose of S lowered plasma insulin by 85%. In the cat, a similar infusion of S lowered basal plasma insulin concentration by 87%, but its depressive effect during .alpha.-adrenergic blockade was comparatively less pronounced (68%) than in the rat. In the mouse, a single i.v. injection of S induced a short-lasting depression of plasma insulin concentration during .alpha.-adrenergic blockade. S apparently does not inhibit insulin release simply by stimulation of .alpha.-adrenoceptors on the .beta.-cell. It cannot be ruled out, however, that a more complex interaction exists between S and the sympatho-adrenal system with regard to the control of insulin secretion.

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