Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of various polypeptide enterohormones and the tachykinin secretogogue, physalaemin, on electrolyte transport by the main excretory duct of the mandibular gland of the rabbit were studied in vitro. Vasoactive intestinal peptide (VIP, 2 X 10(-11) mol 1(-1)) and gastric inhibitory polypeptide (GIP, 10(-11) mol 1(-1)) reduced nett Na+ movement from lumen to interstitium and VIP also reduced the transepithelial potential difference; the effective concentrations of the two hormones lay within the range of normal plasma concentrations. Gastrin (5 x 10(-7) mol 1(-1)) and synthetic secretin (2 x 10(-7) mol 1(-1)) had similar effects but only at concentrations well above the normal plasma levels. Caerulein, an analogue of the octapeptide of cholecystokinin, had no effect on duct function even at a concentration of 10(-6) mol 1(-1). The potent salivary secretogogue, physalaemin (4 x 10(-8) mol 1(-1)), which is an analogue of Substance P, a putative mammalian enterohormone and neurotransmitter substance, caused a marked increase in ductal Na transport (in rat as well as rabbit). It is concluded that VIP and GIP would normally play a role in determining salivary electrolyte composition and it is postulated that their action may be antagonized by a tachykinin such as Substance P.
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PMID:Modification of salivary duct electrolyte transport in rat and rabbit by physalaemin, VIP, GIP and other enterohormones. 56 44

Many studies suggest that smooth muscle relaxation caused by beta-adrenergic agents and various neuropeptides occurs as a result of an increase in cellular adenosine 3',5'-cyclic monophosphate (cAMP). However, the evidence is indirect, and furthermore does not demonstrate that an increase in cAMP is essential for mediating relaxation. To define more clearly the role of cAMP in receptor-mediated smooth muscle relaxation, we used a specific competitive antagonist of the action of cAMP on protein kinase A, (R)-p-adenosine 3',5'-cyclic phosphorothioate [(R)-p-cAMPS], and its S isomer, (S)-p-cAMPS, which functions as a cAMP agonist. In gastric smooth muscle cells from guinea pig, (S)-p-cAMPS caused a dose-related relaxation [50% inhibitory concentration (IC50) 86 +/- 59 nM]. Vasoactive intestinal peptide (VIP) produced smooth muscle cell relaxation (IC50 2.3 +/- 0.8 nM) through occupation of specific VIP receptors. (R)-p-cAMPS inhibited VIP-induced relaxation, with a rightward shift in the VIP dose-response curve, suggesting competitive antagonism. Furthermore, (R)-p-cAMPS inhibited relaxation induced by other agents that increase cellular cAMP (isoproterenol, calcitonin gene-related peptide, and glucagon) but not that induced by ATP or sodium nitroprusside. (R)-p-cAMPS had no effect on contraction stimulated by carbachol, cholecystokinin, or substance P. These data demonstrate that activation of protein kinase A is primarily responsible for mediating gastrin smooth muscle relaxation produced by adrenergic agents and various neuropeptides.
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PMID:A primary role for protein kinase A in smooth muscle relaxation induced by adrenergic agonists and neuropeptides. 132 27

The role of neuropeptides in the regulation of macromolecule secretion from human nasal mucosa is incompletely understood. Previous in vitro explant culture studies have demonstrated the effects of neuropeptides on lactoferrin release from serous cells and 3H-glucosamine labeled respiratory glycoconjugate secretion from mucus-containing cells. The generation of a new monoclonal antibody, 7F10, has led to the development of an ELISA for high molecular weight respiratory mucous glycoproteins (MGP). This ELISA was used to measure the ability of sensory, parasympathetic and sympathetic neuropeptides to stimulate MGP release from human nasal mucosal fragments in short term explant culture in vitro. Significant MGP release was stimulated by the sensory neuropeptides gastrin releasing peptide (10 microM GRP: 10.6% +/- 2.4% increase, n = 8, P less than 0.01 vs. control), substance P (1 microM SP: 12.5% +/- 5.4%, n = 11, P less than 0.05), neurokinin A (1 microM NKA: 17.8 +/- 4.3%, n = 6, P less than 0.01), while calcitonin gene related peptide (CGRP) was without effect. Vasoactive intestinal peptide (VIP), a neurotransmitter from parasympathetic nerves, induced significant dose dependent MGP secretion, but had no additive or inhibitory interaction with methacholine-induced secretion. Neuropeptide Y (NPY), present in sympathetic nerves, had no effect on MGP secretion. These observations correlate with the effects of neuropeptides on serous cell lactoferrin secretion, and the presence of specific GRP, SP, and VIP binding sites on human nasal submucosal glands that have been detected by autoradiography. GRP and tachykinins (SP and NKA) from sensory nerves, and VIP released during parasympathetic reflexes may significantly stimulate mucous and serous cell secretion from human nasal mucosa in vivo.
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PMID:The effects of neuropeptides on mucous glycoprotein secretion from human nasal mucosa in vitro. 138 97

The occurrence and distribution of an array of neuropeptides and dopamine-beta-hydroxylase in the circumvallate papillae of monkey, pig, cow, ferret, cat, rat and mouse was studied by immunocytochemistry. The animals were chosen to represent species with different diets. Substance P/neurokinin A- and calcitonin gene-related peptide-containing fibers were numerous in the circumvallate papillae of all animals examined, with the highest frequency in monkey, pig, cow, rat and mouse; in ferret and cat moderate numbers were detected. Vasoactive intestinal peptide/peptide histidine isoleucine amide-containing fibers were numerous in the circumvallate papillae of pig, while they were moderate in number in monkey, ferret and mouse. Neuropeptide Y-containing fibers were few to moderate in number in the circumvallate papillae of all species. Galanin-containing fibers were numerous in the pig circumvallate papillae, while only a few fibers could be detected in monkey, cow, cat, rat and mouse. Somatostatin-containing fibers were seen only in the cat circumvallate papillae, gastrin-releasing peptide-containing fibers in the cow and cat, cholecystokinin/gastrin-containing fibers in the pig and cow. Dopamine-beta-hydroxylase-containing fibers were detected in all animals studied. They were few to moderate in number in the circumvallate papillae. There was no obvious link between the peptidergic innervation pattern and the food habits.
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PMID:Peptide-containing nerve fibers in the circumvallate papillae. 169 15

Somatostatin (SRIF), cholecystokinin (CCK), gastrin and substance P, as single agents, do not influence baseline cellular cAMP levels in human thyroid cultures. SRIF inhibits TSH-induced cAMP accumulation in human thyroid cell, while CCK, gastrin and substance P do not modify cAMP response to TSH. Vasoactive intestinal peptide (VIP) increases cellular cAMP levels in human thyroid cultures and its effect is additive to increases produced by norepinephrine (NE) and isoproterenol (ISO). Neither SRIF nor the other tested peptides influence adrenergic and VIP-ergic cAMP stimulation.
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PMID:Neuropeptidergic control of cyclic AMP accumulation in human thyroid cell. 241 54

The effects of various biologically active peptides on net jejunal water and electrolyte fluxes were studied in dogs in vivo. Vasoactive intestinal peptide (VIP), gastric inhibitory polypeptide (GIP), glucagon, gastrin, bombesin and neurotensin all had secretagogue activity, while methionine enkephalin stimulated net absorption. Somatostatin had no effect on net basal water and electrolyte transport, but inhibited glucagon-stimulated secretion. Secretin, calcitonin, substance P and pancreatic polypeptide (PP) did not have any effect on net water and electrolyte transport in the doses used in these experiments. The precise role played by these peptides in the control of intestinal transport has still to be determined. Studies in man have confirmed that food in the proximal small bowel stimulates secretion at sites remote from the application of food, and abnormal secretion of some peptides (e.g. VIP) has been associated with diarrhoea. Somatostatin has been used successfully to reduce the volume of certain types of secretory diarrhoea. Methods used in these experiments have been applied to the study of the composition and absorption characteristics of solutions used for oral rehydration in diarrhoea and in exercise-induced dehydration. Glucose polymers have been shown to be absorbed as rapidly as glucose from the jejunum.
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PMID:The effect of luminal and hormonal factors on small intestinal water and electrolyte transport. 287 15

Somatostatin is located predominantly in D-cells of the antral and fundic area of the stomach and in the duodenal bulb. Furthermore, somatostatin is contained in neurons of the extrinsic and intrinsic nervous system. Somatostatin inhibits gastric acid, pepsin and gastrin secretion, and it stimulates gastric mucous secretion. All in all, somatostatin could exert protection of the gastric mucosa by reduction of aggressive and augmentation of protective mechanisms. There is, however, no evidence for a role of somatostatin in the pathogenesis of peptic ulcer. Endogenous opioids which have to be considered as potential peptidergic neurotransmitters increase vagal and postprandial gastric acid secretion and accordingly cannot be considered as a protective factor. Vasoactive intestinal peptide (VIP), also a peptidergic neurotransmitter, reduces acid and stimulates mucous and bicarbonate secretion. If this is of physiological relevance remains to be established. Secretin might be a protective factor for the gastric mucosa by stimulating mucous and bicarbonate secretion. On the other hand, it augments pepsin secretion which might attenuate any potential protective effects of secretin.
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PMID:[Somatostatin and opioids, secretin and VIP--protectors of the mucosa?]. 288

We hypothesized that bioactive peptides might be released into the portal circulation and mediate pathophysiologic alterations accompanying small bowel obstruction. We studied this question in a subacute canine small bowel obstruction model using 50 percent diameter occlusion. Control animals underwent sham laparotomy. Vasoactive intestinal peptide (VIP), peptide YY, and gastrin were measured in portal and systemic plasma by specific radioimmunoassays at 24-hour intervals as the obstruction progressed to completion over 5 days. All peptides in both groups demonstrated portal and peripheral gradients. In control dogs, peptide concentrations did not change postoperatively but VIP increased markedly in obstructed dogs, demonstrating a median portal level of 95 pmol/liter at 96 hours compared with 31.5 pmol/liter in control animals. These portal VIP levels are known to cause hypersecretion and splanchnic vasodilation in experimental models. The release of vasoactive compounds such as VIP may mediate local pathophysiology in human small bowel obstruction. A similar explanation of the systemic effects is consistent with the known cardiopulmonary bioactivity of VIP.
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PMID:Does vasoactive intestinal polypeptide mediate the pathophysiology of bowel obstruction? 291 Jan 15

The effects of intracerebral injections of brain-gut peptides in the preoptic region on the secretion of luteinizing hormone (LH) and prolactin (PRL) were examined in ovariectomized, estrogen-primed rats. Gastrin or cholecystokinin-octapeptide injection in the preoptic region induced a moderate increase of circadian rise of LH secretion in some animals but no appreciable change in PRL secretion. Secretin injection was strikingly effective in increasing circadian rise of LH and PRL secretion. Vasoactive intestinal peptide injection completely abolished the occurrence of circadian rise of LH secretion whereas PHI injection facilitated LH secretion undergoing the circadian rhythm. The results suggest that those peptides act as neurotransmitters or neuromodulators in the preoptic region and are implicated in the regulation of LH and PRL secretion.
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PMID:Effects of preoptic injections of gastrin, cholecystokinin, secretin, vasoactive intestinal peptide and PHI on the secretion of luteinizing hormone and prolactin in ovariectomized estrogen-primed rats. 359 40

The effect of synthetic human gastrin I, infused at two doses, on the concentrations of somatostatin, pancreatic polypeptide, and vasoactive intestinal peptide in portal and systemic blood was studied in six anesthetized dogs. Intragastric pH was maintained at 5.5, and acid output was measured by intragastric titration. Significant increases in somatostatin and pancreatic polypeptide concentrations in portal blood were found with the lower dose of gastrin (0.5 microgram/kg . h) infused for 40 min. When gastrin was infused at 1.5 microgram/kg . h for 100 min, both portal and systemic blood concentrations of somatostatin and pancreatic polypeptide rose significantly. Cimetidine (300 mg, as an iv bolus), given 40 min after the beginning of the second infusion, did not affect gastrin-stimulated release of somatostatin and pancreatic polypeptide, whereas acid output was completely abolished. Vasoactive intestinal peptide concentrations did not change with the infusion of either dose of gastrin. This daily shows that gastrin releases somatostatin and pancreatic polypeptide in a dose-dependent fashion, and since this release was not acid mediated, it appears likely to be a direct action of gastrin.
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PMID:Effects of gastrin on circulating levels of somatostatin, pancreatic polypeptide, and vasoactive intestinal peptide in dogs. 610 2


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