Peptidergic and nitrergic inhibitory neurotransmissions in the hamster jejunum: Regulation of vasoactive intestinal peptide release by nitric oxide

Regulation of vasoactive intestinal peptide (VIP) release by nitric oxide (NO) was investigated in the hamster jejunum. Electrical field stimulation and applied NO (3-100 muM) evoked biphasic hyperpolarizations consisting of an initial transient hyperpolarizing component followed by a second more slowly developing component (late component), The NO synthase inhibitor N-G-nitro-L-arginine methyl ester (200 muM) abolished the biphasic inhibitory junction potential evoked by electrical field stimulation. The NO scavenger oxyhemoglobin (50 muM) and the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ; 10 muM) abolished both components of the inhibitory junction potentials and the NO-induced hyperpolarizations. VIP(6.28) (1 muM). which abolished VIP (3 muM)-induced hyperpolarizations, also inhibited the late components of the inhibitory junction potentials and the NO-induced hyperpolarizations. ODQ inhibited VIP release and cAMP production by electrical field stimulation and NO application, N-6-2,0-Dibutyryladenosine 3',5'-cyclic monophosphate (0.1-3 muM) caused a membrane hyperpolarization. These results suggest that NO may stimulate VIP release from enteric nerves in the hamster jejunum. In addition, we propose that NO and NO-stimulated VIP contribute to the early and late components of the inhibitory junction potentials. respectively, in the circular smooth muscle cells of the hamster jejunum. (C) 2002 IBRO. Published by Elsevier Science Ltd. All rights reserved.