Peptidergic and nitrergic inhibitory neurotransmissions in the hamster jejunum: regulation of vasoactive intestinal peptide release by nitric oxide
Section snippets
Tissue preparation
Male Syrian hamsters (80–120 g) were obtained from SLC (Japan) and were anesthetized with diethyl ether and exsanguinated via the carotid arteries. Tissue preparations and electrophysiological techniques were similar to those previously described (Matsuyama et al., 1999b). After the abdominal cavity was opened, a length of about 3–4 cm of jejunum was removed and immediately immersed in physiological salt solution (PSS; see below) at room temperature. The contents of the excised segment were
Membrane potential responses to electrical field stimulation
The circular smooth muscle cells of the hamster jejunum displayed either electrical quiescence (in 74/248 cells) or spontaneous rhythmic potentials (in 174/248 cells), which represented slow wave activity. Quiescent cells had an average resting membrane potential of −44.2±0.3 mV, while the most negative potential between the slow waves in unquiescent cells was −47.5±0.2 mV. There was no significant difference between the average resting membrane potentials of the quiescent cells and most
Discussion
The results of the present study suggest that the induction of VIP release by NO contributes to the late components of the IJPs and hyperpolarizations in the hamster jejunum. These conclusions are supported by the following observations: (i) the late components of the nitrergic IJPs and the NO-induced hyperpolarizations were inhibited by VIP(6–28) and ODQ; (ii) EFS-stimulated VIP release was inhibited by L-NAME; (iii) VIP release produced by EFS and NO application was abolished by ODQ; and (iv)
Conclusion
In conclusion, our studies suggest that NO and NO-stimulated VIP are involved in the early and late components of the nitrergic IJPs, respectively, in the hamster jejunum. Furthermore, we propose that endogenous and exogenous NO cause membrane hyperpolarization not only via production of cGMP but also by VIP released from enteric nerves which in turn produces cAMP in the hamster jejunum.
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