Somatostatin mediates bombesin inhibition of chloride secretion by rectal gland

Abstract

The function of bombesin-like peptide, a neurotransmitter present in nerve fibers of elasmobranch rectal glands, is unknown. Since the principal activity of the rectal gland is to secrete chloride, the effects of bombesin on chloride secretion and the role of somatostatin in this response was studied. Bombesin failed to stimulate secretion in rectal glands perfused in the basal state. When added to glands stimulated by a constant infusion of vasoactive intestinal peptide (VIP), bombesin (8 x 10(-7) M) reversibly inhibited chloride secretion by 56 +/- 9.7% and at the same time evoked a 10-fold increase in the liberation of somatostatin into the venous effluent. Inactivation of somatostatin by the addition of cysteamine partially suppressed the inhibitory effect of bombesin on glandular secretion. The effect of bombesin to reduce chloride secretion was completely prevented by the calcium channel blocker nifedipine, which inhibits neurotransmitter release. These results suggest that bombesin inhibits the effect of VIP to stimulate chloride secretion by releasing somatostatin from neurosecretory nerve terminals within the rectal gland.