Ellis J L, Farmer S G
Nova Pharmaceutical Corporation, Baltimore, Maryland 21224-2788.
Pulm Pharmacol. 1989;2(2):107-12. doi: 10.1016/0952-0600(89)90032-x.
There is increasing evidence that vasoactive intestinal peptide (VIP) and peptide histidine isoleucine (PHI) are non-adrenergic, non-cholinergic (NANC) inhibitory neurotransmitters in airway smooth muscle. The possibility that VIP and PHI may also have neuromodulatory effects on excitatory responses, mediated by cholinergic nerves, to electrical field stimulation (EFS) was studied in guinea-pig isolated trachea. VIP (0.5 nM) pre-junctionally, inhibited the release of acetylcholine (ACh), whereas post-junctionally, responses to methacholine (MCh) were enhanced. At a maximum relaxant concentration (100 nM), VIP inhibited cholinergic neurotransmission both pre- and post-junctionally. Similarly, PHI (30 nM) inhibited neuronal ACh release, but enhanced transmitter action post-junctionally. At 3 microM, PHI inhibited ACh release. VIP- and PHI-induced inhibition of EFS was not affected by methysergide, pyrilamine, naloxone, phentolamine and propranolol. These data suggest that, in airway smooth muscle VIP and PHI may modulate cholinergic transmission via specific receptors.
越来越多的证据表明,血管活性肠肽(VIP)和肽组氨酸异亮氨酸(PHI)是气道平滑肌中的非肾上腺素能、非胆碱能(NANC)抑制性神经递质。在豚鼠离体气管中研究了VIP和PHI是否也可能对由胆碱能神经介导的电场刺激(EFS)的兴奋性反应具有神经调节作用。VIP(0.5 nM)在接头前抑制乙酰胆碱(ACh)的释放,而在接头后增强对乙酰甲胆碱(MCh)的反应。在最大舒张浓度(100 nM)时,VIP在接头前和接头后均抑制胆碱能神经传递。同样,PHI(30 nM)抑制神经元ACh释放,但在接头后增强递质作用。在3 μM时,PHI抑制ACh释放。VIP和PHI诱导的EFS抑制不受麦角新碱、吡苄明、纳洛酮、酚妥拉明和普萘洛尔的影响。这些数据表明,在气道平滑肌中,VIP和PHI可能通过特定受体调节胆碱能传递。