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Role of Vasoactive Intestinal Peptide in Myocardial Ischemia Reperfusion Injury
Published in Sami I. Said, Proinflammatory and Antiinflammatory Peptides, 2020
Dipak K. Das, Nilanjana Maulik, Richard M. Engelman
Vasoactive intestinal peptide (VIP) is a 28-amino acid neuropeptide with diverse physiological properties. Originally isolated from porcine upper intestine (1), it is now known to be present in neural and many other tissues including heart, lung, brain, colon, and genitourinary tract (2). It is abundantly present in neurons of the myenteric plexus that project into circular muscle and specialized longitudinal muscle (3). VIP also causes relaxation to the muscle strips (4). This peptide has been found to exist in the postganglionic nerve terminals in the heart (5). The origins of the VIP immunoreactive nerve fibers are primarily intrinsic, but to some extent also extrinsic (6).
The Airway and Vasoactive Intestinal Peptide Autoantibodies and Receptors
Published in Devendra K. Agrawal, Robert G. Townley, Inflammatory Cells and Mediators in Bronchial Asthma, 2020
Receptors for VIP are widely distributed.25 Since asthma does not usually involve dysfunction of organ systems other than airways, a generalized defect in VIP receptors is unlikely in asthma patients. Local dysfunction of VIP receptors is conceivable. For example, excessive release of VIP in the airways could result in receptor down-regulation. Another possibility arising from detection of VIP autoantibody in asthmatics is that these individuals also have autoantibodies directed against the VIP receptor. This is based on the theory that an idiotypic antibody regulating the synthesis of VIP antibody would be directed against the binding site on the VIP antibody, which is likely to resemble the binding site on the VIP receptor.35,36 The idiotypic anti-VIP antibody would act as a VIP receptor antibody, therefore. In experimental insulin-resistant diabetes, antibodies to insulin and insulin receptors appear in a cyclic, alternating fashion.35 A VIP receptor antibody, if present, may block the binding of VIP to receptors, accelerate receptor internalization, or mediate immune lysis of receptorbearing cells, analogous to the actions of other receptor antibodies.
Other Sleep Modulators
Published in Shojiro Inoué, Biology of Sleep Substances, 2020
Riou et al.35,36 first reported the marked sleep-enhancing activity of VIP in rats. The effects of VIP were dependent on the dosage and the time of day. A single i.c.v. injection of VIP in the morning at a dose of 100 ng induced a significant increase in PS at the expense of wakefulness during an 8-h, diurnal postinjection period. The 15% increase in the amount of PS was due to an increase in the number of PS episodes. A lower dose (10 ng) of VIP increased diurnal wakefulness 17%, but the difference was not significant. A higher dose (1 μg) of VIP exerted no sleep-modulatory effect immediately, but it significantly increased diurnal PS and decreased diurnal wakefulness on the next day. It is interesting that the i.c.v.
Zhizhu decoction alleviates slow transit constipation by regulating aryl hydrocarbon receptor through gut microbiota
Published in Pharmaceutical Biology, 2023
Yong Wen, Yu Zhan, Shiyu Tang, Fang Liu, Rong Wu, Pengfei Kong, Qian Li, Xuegui Tang
The ENS is an important part of the digestive tract (Furness 2012). The excitatory and inhibitory nerves jointly constitute the enteric neural network, which is involved in the regulation of intestinal physiology, including peristalsis (Spencer and Hu 2020). Ach is the most important excitatory neurotransmitter in ENS, which can stimulate gastrointestinal smooth muscle contraction and gland secretion, and promote intestinal peristalsis (Biancani et al. 1988). SP is an excitatory neurotransmitter of the tachykinin family, which can activate Ach and induce smooth muscle contraction, acting as a regulator of Ach (Turner et al. 2007). Studies have shown that there is a significant decrease in the synthesis and release of Ach and SP neurons in the colon tissues of STC patients compared to normal controls (Wattchow et al. 2008; Yik et al. 2011). 5-HT, an important neurotransmitter and paracrine signaling molecule, participates in the regulation of gastric motility through the gastrointestinal smooth muscle contraction mediated by a variety of 5-HT receptors (Gershon and Tack 2007). In addition, VIP is an inhibitory neurotransmitter, which has the function of dilating gastrointestinal sphincter, and the increase of VIP can inhibit gastrointestinal movement (Iwasaki et al. 2019). The present study found that ZZD significantly increased the expressions of Ach, SP, and 5-HT, and decrease the expression of VIP in the colon of STC mice. Serum metabolomics further confirmed that the regulation of ZZD on gastrointestinal function in STC mice may be exerted through regulating neurotransmitters in ENS.
Changes in esophagus interstitial cells of Cajal in response to acute stress
Published in Scandinavian Journal of Gastroenterology, 2022
Zhen-peng Huang, Hu Qiu, Ke Wang, Jia-wei He, Hang Chen, Ling-wang Kong, Yue Zou
Pro-inflammatory factors, such as IL-9, and hormones, including CCK and VIP, all contribute to the growth and development of ICCs. IL-9 is a multifunctional cytokine secreted by cells and can promote cell growth and proliferation. It can also promote the growth of ICCs and help maintain their functions by reinforcing CCK-8S-induced [Ca2+]i increases in ICCs [29]. IL-9 has been shown to be upregulated in airway inflammation [30]. In this study, the airway inflammation seen after lung injury also led to increases in IL-9 levels. CCK is released from mucosal endocrine cells, and it acts not only on the CCK-AR in smooth muscle cells but can also have a direct effect on the ICCs to evoke muscle contraction mediated by CCK-AR and CCK-8 [31]. VIP is released from gastrointestinal tract muscle and is thought to be an index of nitric oxide (NO) production [32]. In the acute stress state, IL-9, CCK and VIP are all rapidly released and then promote the development and growth of lower esophageal ICCs.
Vasoactive intestinal peptide-oma causing refractory diarrhea in a young woman
Published in Baylor University Medical Center Proceedings, 2020
Nagasri Shankar, Catherine Linzay, Kyle Rowe
Although it mainly functions as a neurotransmitter, VIP is also produced by pancreatic islet cells. VIP binds to G protein–coupled receptors on enteric smooth muscle and enterocytes, resulting in cyclic adenosine monophosphate–mediated stimulation of chloride secretion with simultaneous inhibition of sodium chloride absorption.6 This results in large-volume secretory diarrhea, vasodilation, smooth muscle relaxation, and excess biliopancreatic secretion. The diarrhea of VIPoma is typically >3 L per day but can exceed 8 L.1 This leads to marked hypokalemia and metabolic acidosis, thus earning the title “watery diarrhea with hypokalemia and achlorhydria” syndrome, also known as WDHA or Verner-Morrison syndrome. Diarrheal volumes <700 cc per day exclude this syndrome.