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Vasoactive intestinal peptide (VIP) is one of the neurotransmitters which is mainly released by intestinal neurons and is also abundant in the central nervous system (CNS), which is an important brain-gut peptide. There are also many VIP nerve fibers in the pancreas. Fat meal and vagal nerve stimulation can induce the release of VIP. The active peptide is a kind of straight chain peptide extracted from small intestinal mucosa. It is arranged as a part of glucagon and secretin, which can reduce blood pressure by vasodilation. From the hepatic artery, the visceral vessel has a strong action ability, but has no effect on the femoral artery. It has a strong promoting effect on the secretion of intestinal fluid, but it has a weak effect on the secretion of pancreas. It can inhibit the secretion of gastric juice and inhibit the contraction of digestive tract smooth muscle.
Vasoactive intestinal peptide (VIP) plays its biological role by activating two kinds of specific membrane receptors: VPAC1 and VPAC2, which belong to II G protein-coupled receptor (GPCRs). It consists of seven transmembrane α helical structures and short peptides in and out of cells. VPAC stimulated by VIP activated adenylate cyclase in a dose-dependent manner, then increased the concentration of cAMP in cells. The activation of VPAC also increased the concentration of Ca2+ and regulated the activity of phospholipase D in cells. In addition to binding to VPAC, VIP could also bind to the pituitary adenylate cyclase activating peptide (PAC1), a specific receptor, with low affinity.
VIP and VPAC are widely expressed and distributed in vivo and produce a variety of important biological effects, suggesting that VIP/VPAC is a valuable target molecule for drug development. Past studies have suggested that VIP is a potential therapeutic agent for asthma, impotence, stroke, chronic inflammation, neurodegenerative diseases and tumors. Among the many roles of VIP, anti-inflammatory and neuroprotection are the two most promising therapeutic areas.
Reference
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