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At least 1,639 records · Page 91Linked to original sources
PubMed2002

Absent secretion to vasoactive intestinal peptide in cystic fibrosis airway glands.

We are testing the hypothesis that the malfunctioning of airway gland serous cells is a component of cystic fibrosis (CF) airway disease. CF is caused by mutations that disrupt CF transmembrane conductance regulator, an anion channel essential for proper fluid secretion in some epithelia. Submucosal glands supply most of the mucus in upper airways, and gland serous cells are the primary site of CF transmembrane conductance regulator expression in airways. We have discovered a major defect in CF glands by in situ optical monitoring of secretions from single human airway glands. CF glands did not secrete to agents that elevated [cAMP](i) (0 responses/450 glands, 8 subjects), whereas glands were responsive in all donor tracheas (605/827 glands, 15 subjects) and in bronchi from subjects who were transplanted because of other lung diseases (148/166 glands, n = 10). CF glands secreted to cholinergic stimulation, and serous cells were abundant in glands from all CF subjects. The complete absence of secretion to agents that elevate [cAMP](i) suggests that altered secretion of gland mucus could contribute to CF lung disease.

Adult↗
PubMed1994

Sepsis increases production of total secreted proteins, vasoactive intestinal peptide, and peptide YY in isolated rat enterocytes.

The effect of sepsis on the synthesis of endogenous and secretory proteins, including vasoactive intestinal peptide (VIP) and peptide YY (PYY), was determined in enterocytes from jejunum of rats. Sepsis was induced by cecal ligation and puncture (CLP). Control rats were sham-operated. Total endogenous and secreted protein synthesis was assessed in incubated jejunal enterocytes by measuring incorporation of 3H-phenylalanine into protein. Release of VIP and PYY into the medium of incubated enterocytes and cellular levels of the gut peptides were measured by radioimmunoassay. Sixteen hours after CLP, synthesis rates of both endogenous and secreted proteins were increased, and this effect of sepsis was most pronounced in cells from the lower parts of the villi and crypts. Enterocytes from septic rats released more VIP and PYY into the incubation medium, and approximately half of the peptides they released were newly synthesized VIP and PYY. Intracellular levels of VIP and PYY were increased as early as 4 hours after induction of sepsis. Our results suggest that sepsis stimulates the synthesis of endogenous and secretory proteins, including certain gut peptides, in small intestine mucosa. This is consistent with previous observations of increased circulating levels of VIP, PYY and other gastrointestinal hormones during sepsis. The biological significance of increased synthesis of gut peptides and other intestinal proteins during sepsis remains to be determined.

Analysis of Variance↗
PubMed1999

Neurotransmitters modulate cytokine-stimulated interleukin 6 secretion in rat intestinal smooth muscle cells.

BACKGROUND & AIMS: Cytokine production by resident cells of the richly innervated muscularis externa may contribute to neuromuscular changes observed during intestinal inflammation. This study investigated neurotransmitter modulation of cytokine production by intestinal smooth muscle. METHODS: We measured interleukin (IL)-6 messenger RNA expression by reverse-transcription polymerase chain reaction, IL-6 by bioassay, and cyclic adenosine monophosphate by enzyme immunoassay in rat cultured intestinal smooth muscle cells exposed to IL-1beta, in the presence or absence of neurotransmitters. RESULTS: IL-1beta significantly increased IL-6 messenger RNA and protein. This was dose-dependently enhanced by vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), and norepinephrine and inhibited by [LYS1,PRO2,5,ARG3,4,TYR6]VIP and propranolol, respectively. Forskolin mimicked the stimulatory effects of these neurotransmitters on IL-6 secretion, and the protein kinase inhibitor6-22 amide abolished the actions of VIP, CGRP, and norepinephrine, but not that of human recombinant IL-1beta, on IL-6 secretion. These agents each increased cyclic adenosine monophosphate activity in muscle substance P, and the neurokinin 1 agonist Ac-[Arg6,Sar9,Met(O2)11] substance P(6-11) inhibited the IL-1beta-induced IL-6 release. CONCLUSIONS: This study shows neuropeptide and sympathetic modulation of IL-1beta-induced IL-6 production by intestinal smooth muscle. These interactions may contribute to altered muscle function during intestinal inflammation.

Adrenergic beta-Antagonists↗
PubMed1995

Stereospecific effects of fatty acids on proglucagon-derived peptide secretion in fetal rat intestinal cultures.

The ingestion of fats is a potent stimulus for the secretion of the proglucagon-derived peptides (PGDPs), including the insulinotropic peptide glucagon-like peptide-1 from the intestinal L cell. The aim of the study was to characterize the structural requirements for fatty acid-induced secretion of the PGDPs and investigate the cellular mechanisms through which fatty acids mediate PGDP secretion. Fetal rat intestinal cell cultures were incubated with 10-150 microM fatty acids that differed in chain length (14-18 carbons) and degree of unsaturation (0-2). Inhibitors of protein kinase C (PKC) and fatty acid esterification and oxidation were also incubated with the cells in the presence of stimulatory fatty acids. The cultures were assayed for glucagon-like immunoreactivity and glucagon-like peptide-1-(7-36)NH2 secretion. Monounsaturated fatty acids of chain length greater than 14 carbons stimulated PGDP secretion by 1.8 to 3.4-fold in a dose-dependent fashion (P < 0.05 to P < 0.001). Enhanced PGDP secretion was lost upon full saturation of the stimulatory fatty acids. Furthermore, although blockade of fatty acid esterification with a carboxyl methyl ester group prevented PGDP secretion, inhibition of fatty acid oxidation with methyl palmoxirate did not prevent PGDP secretion. Finally, the use of various inhibitors of PKC (staurosporine, H7, 24-h down-regulation) also did not alter fatty acid-induced PGDP secretion. In conclusion, monounsaturated long-chain fatty acids possessing a free carboxyl group stimulate intestinal PGDP secretion. Neither fatty acid oxidation nor classical isoforms of PKC appear to be directly involved in this response. Therefore, the structure of the fatty acid plays a central role in inducing intestinal PGDP secretion. These findings suggest that fat composition may significantly affect the magnitude of the GLP-1 response to ingested nutrients.

Animals↗
PubMed1982

Stimulation of renin secretion by vasoactive intestinal peptide.

Vasoactive intestinal peptide (VIP) increased plasma renin activity (PRA) in pentobarbital-anesthetized dogs. A 15-min infusion of VIP directly into the renal artery at a dose of 33 ng . kg-1 min-1 increased renin secretion rate from 1,461 +/- 393 to 5,769 +/- 1,794 ng ANG I . ml-1 . 3 h-1 . min-1, and increased PRA from 19.2 +/- 2.3 to 29.2 +/- 4.7 ng ANG I . ml-1 . 3 h-1. Renal blood flow and creatinine clearance were also increased, whereas plasma potassium concentration and diastolic blood pressure decreased. There was no change in sodium or potassium excretion. When administered intravenously, 33 and 13 ng . kg-1 . min-1 VIP increased PRA. A dose of 3.3 ng . kg-1 . min-1 failed to increased PRA when given intravenously but produced a significant increase in PRA from 22.8 +/- 8.1 to 40.5 +/- 19.4 ng ANG I . ml-1 . 3 h-1 when infused into the renal artery. This increase occurred without any change in plasma potassium concentration or blood pressure. Renin secretion was increased by a two- to threefold increase in plasma VIP; comparable increases in plasma VIP have been reported to be produced by various experimental procedures. The data indicate that VIP increases renin secretion. The peptide appears to act directly on the kidney and may act directly on the juxtaglomerular cells.

Animals↗
PubMed1982

Effect of vasoactive intestinal peptide on gastric secretion in the cat.

The effects of porcine vasoactive intestinal peptide on the acid and pepsin secretions from denervated gastric pouches and innervated stomach were studied in conscious cats both in basal conditions and after stimulation with pentagastrin, histamine, or a liver meal. In contrast with the well-known inhibitory effect of vasoactive intestinal peptide on acid and pepsin secretions in dogs, the peptide induced in cats an increase of the acid and pepsin responses to pentagastrin and an increase of the gastric mucosal blood flow as determined by aminopyrine clearance. Vasoactive intestinal peptide similarly enhanced the acid and pepsin responses to a liver meal in spite of a significant inhibition of the postprandial release of gastrin. The peptide increased the pepsin response but slightly decreased the acid response to histamine. Thus in cats, porcine vasoactive intestinal peptide consistently stimulates pepsin secretion and potentiates the meal- and pentagastrin-induced acid responses.

Animals↗
PubMed1982

Intestinal absorption and secretion of radioactive vanadium (48VO3-) in rats and effect of Al(OH)3.

Vanadium in the metavanadate form (VO3-) is a powerful inhibitor of Na+, K+-ATPase. Because of the similarity between the oxy anions of vanadium and phosphorus, it was of interest to see whether Al(OH)3 would restrict the intestinal absorption of vanadium, as it does that of phosphorus. VO3- was extensively bound to a suspension of Al(OH)3 at pH 5-8. Sprague-Dawley rats (180-300 g) were fasted overnight and gavaged with 5 mumol Na3 VO4 in 1.0 ml 0.9% NaCl containing 1 microCi 48V. Control animals (n = 12) simultaneously received 1.0 ml diluent and experimental animals (n = 12) received 1 ml Al(OH))3. Diluent and Al(OH)3 were then given daily for 4 d. Urine and feces were collected separately each day. In control animals total 48V recovery (stool and urine) over 4 d was 86.6 +/- 2.4% of the administered dose. Although Al(OH)3 insignificantly increased total 48V recovery (93.6 +/- 3.2%), it markedly increased excretion of 48V in the stool as compared to the urine (control: stool, 69.1 +/- 1.8%; urine, 12.5 +/- 1.3%; Al(OH)3: stool, 85.7 +/- 1.5%; urine, 7.9 +/- 1.8%). Animals were then sacrificed and tissue uptake of tracer measured. The pattern of unexcreted 48V in tissue of both groups was kidney greater than bone greater than liver greater than intestine greater than muscle, but the tissue levels were uniformly higher in controls than in Al(OH)3-treated animals. The ability of Al(OH)3 to remove endogenous VO3- was also examined. 48V was injected ip (n = 20). Half of the animals received diluent and half received 1.0 ml Al(OH)3 by gavage daily for 4 d. There were no differences in the pattern of 48V tissue distribution and excretion. It is concluded that Al(OH)3 may prevent tissue accumulation of VO3- from dietary sources by reducing intestinal VO3- absorption.

Aluminum Hydroxide↗
PubMed2001

The influence of active secretion processes on intestinal absorption of salbutamol in the rat.

Salbutamol was perfused in the small intestine of rat using a standard rat gut "in situ" preparation: (1) in inhibitor-free solution at seven different concentrations (0.15, 0.29, 1.20, 5.0, 9.0, 13.0 and 18.0mM); (2) at a 0.29mM concentration - thought to be close to the allometric dose in man - in the presence of a non-specific enzyme inhibitor, sodium azide (0.3, 3.0 and 6.0mM); and (3) at 0.29mM in the presence of a selective secretion inhibitor, verapamil (10.0 and 20.0mM). In free solution, the mixed-order rate constants, k'(a), of salbutamol increase as the solute concentration increases until an apparent asymptotic value is reached. This could be due to the saturation of enzymatic systems responsible for the secretion of the drug from the enterocyte to the luminal fluid, a process that could explain the poor absorption of salbutamol. In the presence of sodium azide, the k(a) values increased about 1.5-fold, whereas in the presence of verapamil they increased two- to three-fold. These results indicate that salbutamol can act as a substrate of an intestinal secretory transport, which probably includes--at least in part--the enzyme P-glycoprotein, since verapamil has been shown to inhibit this enzyme by dose-dependent competition. This leads to a secretion-limited peroral absorption of salbutamol, which contributes to the poor oral bioavailability of the drug. The possible options for improving salbutamol absorption are discussed.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1996

Neural involvement in 5-hydroxytryptamine-induced net electrogenic ion secretion in the rat intestine in-vivo.

5-Hydroxytryptamine (5-HT) induces active electrogenic anion secretion by both the small intestine and the colon, responses that can be detected from measurements of transmural electrical activity. This approach was adopted to examine the involvement of neural mechanisms in 5-HT-induced secretion in rat proximal jejunum, distal ileum and proximal colon in-vivo. Under control conditions, 5-HT caused maximum rises in transintestinal potential difference of 4.7 +/- 0.3, 3.8 +/- 0.4 and 7.6 +/- 0.3 mV, respectively, with corresponding ED50 values of 28 +/- 3, 38 +/- 4 and 41 +/- 4 nmol kg-1 (n = 12). In each region examined a neural component in the secretory response to 5-HT was identified. Hexamethonium (22 mumol kg-1) reduced the 5-HT response in each region: in the jejunum and colon, it also attenuated the responses to the 5-HT3 agonist, phenylbiguanide and to 5-methoxytryptamine (5-MeOT), an agonist at all 5-HT receptors except 5-HT3, indicating that in these regions the nicotinic pathway can be activated by more than one 5-HT receptor subtype. Atropine (0.27 and 2.7 mumol kg-1) was found to have regional effects on the intestinal responses to 5-HT receptor agonists. In the jejunum, evidence for a pro-secretory muscarinic pathway which could be activated by more than one 5-HT receptor subtype was found. In the ileum and colon no muscarinic pro-secretory pathway was identified, indeed in the colon, an anti-secretory pathway may be present. This muscarinic anti-secretory pathway was observed with phenylbiguanide and 5-MeOT, but not 5-HT. Substance P release does not appear to be involved in mediating the intestinal secretory response to 5-HT. 5-HT-induced intestinal anion secretion may involve a direct secretory action on the enterocyte which can be modified by neurally-mediated pro-secretory and anti-secretory pathways, the balance between these processes varying down the length of the gut.

Acetylcholine↗
PubMed1987

[Stimulation of prolactin secretion by vasoactive intestinal peptide].

Dopamine has already been recognized as an inhibiting factor of prolactin. On the other hand, the stimulators of prolactin are still judged diversely at the moment. In addition to hypothalamic TRH, serotonine as well as endogenous opiates and VIP are under discussion. The object of our studies was testing the function of VIP in directing prolactin secretion on three different groups of patients: 1. hyperprolactinaemic women of WHO-group VI; 2. patients who had undergone a TRH-test along with an endocrine check-up; 3. post partum in childbed. The determination was made from analyzing peripheral blood by radioimmunoassay. In 20 amenorrhoeic patients of WHO-group VI, their prolactin and VIP levels were determined between 8 and 10 a. m. Only 4 patients showed a VIP-concentration below 20 pg/ml (which represents the limit of detectability). The other 16 patients showed an increased concentration of VIP. In 15 cases there was an obvious correlation of VIP and prolactin concentrations according to the linear regression. In the course of a TRH-test to 20 and 40 minutes after initial blood examination prolactin and VIP were again determined. After 20 minutes all patients showed a threefold increase of the initial prolactin value. On the other hand, VIP increased in 3 cases only. Apart from all those patients who wanted to become pregnant, these three women--being postmenopausal--showed increased initial values already in the unstimulated condition. The third group of patients consisted of 26 women in childbed. Their prolactin and VIP were determined between the second and eight day post partum.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1999

Is glucagon-like peptide 1 an incretin hormone?

Glucagon-like peptide-1 (GLP-1) was predicted, based on the proglucagon gene sequence. It is synthesised by specific post-translational processing in L cells (lower intestine) and secreted mainly as "truncated" GLP-1 [7-36 amide] in response to nutrient ingestion. Glucagon-like peptide-1 stimulates insulin secretion during hyperglycaemia, suppresses glucagon secretion, stimulates (pro)insulin biosynthesis and decelerates gastric emptying and acid secretion. On intracerebroventricular injection, GLP-1 reduces food intake in rodents. A GLP-1 receptor antagonist or GLP-1 antisera have been shown to reduce meal-stimulated insulin secretion in animals, suggesting that GLP-1 has a physiological "incretin" function (augmentation of postprandial insulin secretion due to intestinal hormones) for GLP-1. In healthy human subjects, exogenous GLP-1 slows gastric emptying. Consequently, postprandial insulin secretion is reduced, not augmented. Thus, a participation of this peptide in the incretin effect of non-diabetic humans has not been definitely proven. Nevertheless, it has potent insulinotropic activity, especially during hyperglycaemia. This suggests new therapeutic options for patients with Type II (non-insulin-dependent) diabetes mellitus. On the other hand, most L cells are located in the lower small intestine. Potent inhibitory actions of GLP-1 on upper gastrointestinal motor and digestive functions (e. g. gastric emptying and acid secretion) in response to nutrients placed into the ileal lumen, argue for a role of this peptide as an "ileal brake". Malassimilation and diarrhea leading to the erroneous presence of nutrients in the lower gut may, via GLP-1, delay gastric emptying and reduce upper gut motility and thereby prevent further caloric losses.

Animals↗