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Results for “Myoelectric Complex, Migrating”

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At least 307 records · Page 17Linked to original sources

PubMed1988

The effect of increased intracranial pressure (ICP) on gastric motility.

This study evaluates the effect of increased intracranial pressure (ICP) on gastric motility. Nine male cats (weight, 4.84 +/- 1.16 kg) were anesthetized with ketamine and underwent laparotomy for placement of bipolar (silver-silver chloride) electrodes on the serosal surface of the gastroesophageal junction (GEJ), antrum, and prepyloric areas of the stomach. At 1 week frontoparietal burr holes were performed with placement of an epidural Fogarty catheter. Migrating myoelectric complexes (MMCs) were evaluated at the GEJ, antrum, and prepyloric areas at varying levels of ICP (baseline and 20, 40, and 60 mm Hg) using balloon inflation. MMCs at the GEJ were triphasic with a period of 4 sec (+/- 1 sec) at baseline levels. At ICP levels above baseline, periodicity and waveforms at the GEJ became irregular. Waveforms became multiphasic with 1- to 2-sec periods and variable amplitudes. In the antral and prepyloric areas, duration and amplitude of the triphasic MMCs was unchanged from baseline. At 60 mm Hg ICP periodicity was significantly altered at both 1 and 2 weeks. MMCs returned to baseline levels with balloon deflation. The data indicate that elevated ICP (to 60 mm Hg) results in consistent and reproducible alterations of MMC periodicity, suggesting that such alterations may influence gastric motility.

Animals↗

PubMed1986

A tetrapeptide isolated from hamster embryo with central opiate properties on gastrointestinal motility but not on pain perception.

The effects of centrally administered kentsin (H-Thr-Pro-Arg-Lys-OH) on intestinal motility and on pain perception were investigated in rats chronically equipped with lateral ventricle catheters. Intestinal motility was recorded electromyographically from electrodes placed on the duodeno-jejunum; analgesia was evaluated by the hot-plate and tail-flick tests. Kentsin (4.0 ug/kg), injected intracerebroventricularly (ICV) 2 hours after the beginning of a meal, restores the "fasted" i.e. the migrating myoelectric complex of intestinal motility, while a 5 times higher dose administered subcutaneously was inactive. The ICV effect of kentsin was blocked by previous ICV administration of naloxone (400 ug/kg). In contrast, kentsin administered ICV (40 ug/kg) or SC (200 ug/kg) did not affect significantly (P greater than 0.05) the time latency in the two analgesic tests during 90 minutes after its administration and did not significantly modify the analgesic effects of (D5-Ala2, Met5) enkephalinamide. We conclude that kentsin when centrally administered acts on opiate receptors to alter gastrointestinal motility but without effects on pain perception.

Animals↗

PubMed1987

Central muscarinic control of the pattern of small intestinal motility in rats.

The effects of central and peripheral administration of muscarinic agonists and antagonists on small intestinal motility were examined in conscious rats chronically fitted with electrodes implanted in the duodeno-jejunal wall and a cannula in a cerebral lateral ventricle. Intracerebroventricular (i.c.v.) administration of either atropine or pirenzepine at doses from 1 to 10 micrograms, 15 min before a 3 and 6 g lab chow meal significantly reduced the duration of the postprandial disruption of the migrating myoelectric complexes (MMC). The reduction was significantly greater for atropine, a mixed M1 and M2 muscarinic receptor antagonist, than for pirenzepine, an antagonist with a high affinity for M1 receptors. At a higher dose (10 micrograms) intra peritoneal (i.p.) administration of atropine or pirenzepine did not modify the postprandial disruption of MMC. Oxotremorine (10 ng) a M2 agonist, but not McNeil A343 (5 micrograms), a selective M1 agonist, given i.c.v. in fasted rats disrupted for 1.5 h the MMC pattern. At the same doses given i.p. oxotremorine and McNeil A343 disrupted the MMC for 15 and 45 min respectively. We conclude that the postprandial changes in the small intestinal motility involve muscarinic receptors, mainly of M2 subtype, at the level of the central nervous system.

Animals↗

PubMed1989

Involvement of platelet-activating factor (PAF) in endotoxin-induced intestinal motor disturbances in rats.

Intestinal myoelectrical activity was investigated in conscious fasted rats chronically implanted with Nichrome electrodes in the duodeno-jejunum. Motility of the small intestine was characterized by the presence of migrating myoelectric complex (MMC) occurring regularly at 16.2 +/- 5.8 minute intervals. Intravenous administration of endotoxin (E. coli S.0111:B4) at a dose of 50 micrograms/kg increased the interval between MMC to 112.6 +/- 26.8 min, the duration of these effects being dose-related between 10 to 100 micrograms/kg. Such a typical myoelectrical alteration, corresponding to rapidly propagated groups of spike bursts, was mimicked by the IP administration of PAF at doses of 10 to 50 micrograms/kg. Previous administration of BN 52021, a specific PAF antagonist at a dose of 50 mg/kg abolished the motor alterations induced by IP injection of PAF (25 micrograms/kg) and significantly (p less than 0.01) reduced by 61.2% those induced by IV endotoxin (50 micrograms/kg). Indomethacin (10 mg/kg IP) as well as SC 19220 (5 mg/kg IV), a PGE2 antagonist, injected prior to endotoxin (50 micrograms/kg IV) or PAF (25 micrograms/kg IP) also reduced significantly (p less than 0.01) the duration of MMC inhibition. It is concluded that endogenous release of PAF is partly responsible for the intestinal motor alterations induced by endotoxin; these effects, strongly reduced after treatment with BN 52021, are also mediated through the release of prostaglandins.

Animals↗

PubMed1996

Effect of motilin, somatostatin and bombesin on gastroduodenal myoelectric activity in sheep.

The effects of motilin, erythromycin, somatostatin and bombesin on antroduodenal myoelectric activity were investigated in conscious sheep. Myoelectric recordings were obtained from electrodes chronically implanted on the antrum and duodenal bulb. Peptides or erythromycin were infused intravenously (i.v.) during 5 min. Antagonists were injected i.v. as a bolus. Neither motilin (2.5-80 ng/kg/min) nor erythromycin (2-16 micrograms/kg/min) modified the antroduodenal myoelectric activity, although a single bolus of these compounds (250 ng/kg and 50 micrograms/kg respectively) increased the antral activity. Somatostatin at 5 ng/kg/min induced a decrease in the myoelectric activity of antrum and duodenum. However, doses of 10 to 40 ng/kg/min evoked a duodenal phase III-like activity with a subsequent quiescence period and a concomitant inhibition of the antral activity. These effects were reproduced by bombesin (2.5 to 40 ng/kg/min). Furthermore, an initial increase in the myoelectric activity and in the frequency of slow waves were recorded in the antrum when the highest doses were used. On the other hand, atropine (0.2 mg/kg) or hexamethonium (2 mg/kg) caused a long-lasting inhibition of antroduodenal myoelectric activity. These cholinergic antagonists abolished the effects induced by somatostatin (20 ng/kg/min) but not those evoked by bombesin but not motilin are putative modulators of the migrating myoelectric complex (MMC) in sheep. Moreover, a cholinergic neural pathway is involved in the somatostatin but not in the bombesin-induced effects.

Animals↗

PubMed1987

Peripheral opioid receptors mediate gastrointestinal secretory and motor effects of dermorphin N-terminal tetrapeptide (NTT) in the dog.

Dermorphin N-terminal-tetrapeptide-amide (NTT) increased both basal and pentagastrin- or histamine-induced secretion in conscious dogs chronically implanted with both gastric fistulae and Heidenhain pouches. These excitatory effects were significantly prevented by the opioid receptor antagonists naloxone and N-methyl-levallorphan-methanesulphonate. In conscious dogs fitted with electrodes and strain-gauges in different parts of gastrointestinal tract, a premature phase III of the migrating myoelectric complex (MMC) in the duodeno-jejunum was triggered by NTT, while the activity of the antrum was not significantly modified. Further, the peptide enhanced the contractile activity of both proximal and distal portions of the colon, including a long-lasting period of increased muscle tone on the distal colon. Either naloxone or N-methyl-levallorphan-methanesulphonate completely prevented motor effects of NTT on gastrointestinal tract. It is concluded that NTT displays significant opiate-like activity on gastric acid secretion and intestinal motility of the dog by activating peripheral mu opioid receptors.

Animals↗

PubMed1994

Central administration of Tyr-MIF-1 stimulates gastrointestinal motility in rats: evidence for the involvement of dopamine, sigma and CCK receptors.

The effect of central administration of the endogenous peptide Tyr-MIF-1 (Tyr-Pro-Leu-Gly-NH2) on the gastrointestinal myoelectric activity and its mechanism of action were studied in rats. Tyr-MIF-1 (40 & 80 micrograms/kg i.c.v.) stimulated antral and duodenal myoelectric activity in a multiphasic manner. On the antrum it induced a primary increase of the frequency of antral spike bursts followed by a consecutive return to control value and a second rise of the frequency. Likewise duodenal migrating myoelectric complexes (MMCs) were initially disrupted and replaced by an irregular spiking activity followed by a reaparition of the phase III of the MMCs with increased amplitude and frequency. Haloperidol (1 mg/kg i.p.) blocked all the effects of Tyr-MIF-1 whereas sulpiride (5 mg/kg s.c.) blocked only the duodenal stimulation without affecting that on the antrum. Similarly BMY-14802 (0.5 mg/kg s.c.) antagonized selectively the primary antral stimulation and the initial disruption of duodenal MMC induced by Tyr-MIF-1. L365 260 (10 micrograms/kg i.c.v.) has also antagonized only the initial disruption of duodenal MMCs. DTG and JO 1784 (100 micrograms/kg i.c.v. each) reproduced fully the effect of Tyr-MIF-1 on the duodenum but not that on the antrum. Domperidone, (+)SCH 23390, devazepide, PK 11-195 and flumazenil did not have effect on the action of Tyr-MIF-1. It is concluded that Tyr-MIF-1 stimulates the antrum involving haloperidol sensitive but nondopamine, dopamine, probably sigma receptors, and the duodenum via a pathway where central D2 dopamine, sigma and CCKB receptors are implied.

Action Potentials↗

PubMed1995

Central effects of neuropeptide FF on intestinal motility in naive and morphine-dependent rats.

The effects on intestinal myoelectric activity of (1DME)Y8Fa (D-Tyr-D-Leu[N-Me]-Phe-Gln-Pro-Gln-Arg-Phe-NH2), a synthetic analog of the neuropeptide FF (Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-NH2) were examined in rats after central (i.c.v.) administration performed before acute morphine and after chronic morphine treatment. The acute administration of morphine sulphate (5 mg/kg s.c.) inhibited the occurrence of intestinal migrating myoelectric complexes (MMC) for 46.0 +/- 15.2 min and increased the number of contractions on the proximal colon (13.5 +/- 2.9 vs 8.1 +/- 0.6/10 min). The duration of the MMC disruption was significantly (P < 0.05) reduced (19.0 +/- 5.6 min) by central administration of naloxone (100 micrograms/kg) but not of (1DME)Y8Fa. In rats rendered tolerant to morphine by injections of a slow-release emulsion containing morphine (75 mg/rat over 48 h), intestinal MMC were disrupted and replaced by a continuous irregular activity. Central administration of naloxone (100 micrograms/kg) restored MMC after having induced for 38.3 +/- 7.3 min a motor pattern typical of the diarrhoeal state, termed minute rhythm. No change in colonic motility was observed despite the occurrence of dirrahoea. The effects of naloxone were reproduced by (1DME)Y8Fa (100 micrograms/kg) that induced a pattern of minute rhythm for 48.9 +/- 15.7 min. These features indicate that neuropeptide FF has no action on the acute effects of morphine on intestinal motility but exerts anti-opioid activities in digestive motor alterations associated to morphine withdrawal.

Amino Acid Sequence↗

PubMed1983

Effects of intracerebroventricular administration of neurotensin, substance P and calcitonin on gastrointestinal motility in normal and vagotomized rats.

The effects of intracerebroventricular (ICV) vs. intravenous (IV) injection of neurotensin, substance P and calcitonin on intestinal myoelectrical activity were examined in fed rats. ICV administered neurotensin and calcitonin restored the 'fasted' pattern of intestinal activity, i.e. the migrating myoelectric complex (MMC) at a dose as low as 12 and 0.2 pmol, respectively, whereas substance P only reduced significantly (P less than 0.01) the duration of the postprandial pattern when injected ICV (48 pmol). Administered systemically at doses 100 times higher than the smallest active doses by the ICV route, calcitonin induced a fasted pattern, while neurotensin and substance P did not modify the fed pattern. The effects of ICV administration of neurotensin and calcitonin were abolished after vagotomy but the shortening effect of substance P on the duration of the postprandial pattern was still present. It is concluded that these three neuropeptides act centrally to control the pattern of intestinal motility in fed rats by shortening the 'fed' pattern for substance P and by restoring the MMC pattern for calcitonin and neurotensin, this last effect being mediated by the vagus.

Animals↗

PubMed1986

Peripheral versus central components of the effects of dermorphin on intestinal motility in the fed rat.

The effects of subcutaneous (s.c.), intraperitoneal (i.p.), intrathecal (i.t.) and intracerebroventricular (i.c.v.) injection of dermorphin (DER) on intestinal myoelectrical activity were examined in fed rats with chronically implanted electrodes on the small and large bowel. DER s.c. restored the 'fasting' pattern of duodenal activity, i.e., the migrating myoelectric complex (MMC), corresponding to an inhibition by about 40% of the fed pattern for 120 min at a dose as small as 0.5 nM per rat. DER i.p. strongly inhibited (about 65%) the fed pattern for 120 min. A fasting pattern lasting 80 min, or a marked inhibition lasting 150 min were recorded after 0.5 nM DER i.t. or i.c.v., respectively. On the contrary, the colonic pattern of activity was inhibited by DER whatever the route used, although the duration of inhibition was different from each other. For both the small and large intestine, similar doses of DER were more efficient by i.c.v. than by i.t. routes, and by i.p. than by s.c. routes. A plurality of sites of action is suggested, including local receptors which are activated, particularly at the duodenal level by i.p. DER (0.5 nM). The supraspinal component of the immediate effects of i.c.v. DER (0.1 nM) were demonstrated by a preferential effect on the colon that was even more intense than after i.t. DER.

Animals↗

PubMed1988

Variations of plasma immunoreactive motilin, pancreatic polypeptide, gastrin and somatostatin along the duodenal motility cycle in the pig.

The peripheral plasma concentrations of immunoreactive motilin, pancreatic polypeptide (PP), somatostatin and gastrin were measured in 7 pigs fasted to 24 h and subsequently fed a standard meal. Plasma motilin peaked during the last part of phase II activity of the migrating myoelectric complex (MMC) sequence (25.2 +/- 2.3 pM), the lowest value being recorded during phase I (10.6 +/- 1.5 pM) after a 24 h fast. Plasma motilin remained at a low level during the digestive pattern of duodenal activity, no fluctuation occurring when the first postprandial MMC recurred. At variance analysis, gastrin and PP were not released phasically with MMC in the fasting state, while at autocovariance both peptides tended to fluctuate during the MMC sequence with positive and negative peaks at regular intervals along MMC cycles. No variation of plasma somatostatin was observed in the fasting animals. These findings argue against a major role of circulating PP, gastrin and somatostatin-like components in the control of fasted and post absorptive duodenal motility in pigs while the role of motilin remains equivocal.

Animals↗

PubMedDate not supplied

Cholinergic role on release and action of motilin.

In conscious dogs with gastric fistula and platinum electrodes on the antrum, duodenum and jejunum, IV atropine 100 micrograms/kg/hr and hexamethonium 10 mg/kg/hr, blocked cyclic increases in fasting plasma motilin concentration (PMC) and spontaneous migrating myoelectric complexes (MMCs) of both antrum and duodenum. The two drugs also blocked occurrence of premature MMCs produced by synthetic porcine motilin. In anesthetized dogs, electrical stimulation of cervical vagi with stimulation parameters: 9 V, 10 c/s, 5 msec, caused a significant increase in both portal and femoral venous PMC which was blocked by atropine. Fractionations of vagus nerve extracts by gel filtration using Sephadex G-50 superfine column revealed most of motilin-like immunoreactivity (MLI) with the same mobility as pure porcine motilin. Studies suggest that cholinergic influence plays a significant role on release of motilin.

Animals↗

PubMedDate not supplied

Peripheral motilin administration stimulates feeding in fasted rats.

Although the physiologic function of the gastrointestinal hormone motilin remains uncertain, plasma levels of this peptide vary with migrating myoelectric complexes (MMCs) in the small intestine. In the fed state, both MMCs and plasma motilin are suppressed. During fasting, cyclical peaks of motilin in plasma occur at the same time as Phase III of the MMC cycle occurs in the duodenum. This dependence of motilin concentrations in plasma on the feeding state of the animal prompted an investigation of the effects of motilin on feeding behavior. Intraperitoneal injection of motilin into fasted, but not fed, rats stimulated eating in a dose dependent manner. A significant stimulation of feeding was seen at doses of 5 and 10 micrograms/kg. Sated rats did not eat whether injected with motilin or vehicle. The feeding response to motilin was blocked by prior injection of the rats with naloxone, naltrexone, or pentagastrin. The dose response suppression of food intake by naloxone was similar in fasted animals treated with motilin or vehicle. Motilin may function as a hunger hormone during periods of fasting.

Animals↗

PubMed1996

Salsalate, morphine, and postoperative ileus.

BACKGROUND: Previously, we demonstrated that ketorolac, a nonsteroidal antiinflammatory drug (NSAID), prevented postoperative small bowel ileus in a rodent model. The aim of this study was to evaluate the effect of salsalate, an NSAID without antiplatelet effect, on postoperative ileus alone or in combination with morphine. METHODS: Forty-eight rats underwent placement of duodenal catheters and were then randomly assigned to one of eight groups (n = 6). Four groups had standardized laparotomy following drug administration, whereas 4 groups underwent the same treatment without laparotomy: control and morphine animals received 0.1 mL alcohol via the catheter, whereas salsalate and salsalate-plus-morphine animals received salsalate (15 mg/kg) dissolved in 0.1 mL alcohol. The animals also received 0.5 mg/kg morphine (morphine and salsalate plus morphine) or the same volume of saline (control and salsalate) subcutaneously. Transit was measured following the injection of a nonabsorbed marker via the duodenal catheter and is defined as the geometric center (GC) of distribution. An additional 20 rats had serosal electrodes placed on the jejunum, and were assigned to one of four treatment groups (control, salsalate, morphine, and salsalate plus morphine; n = 5 each group). Myoelectric activity was recorded until the reappearance of the migrating myoelectric complex (MMC) following laparotomy. RESULTS: Laparotomy and morphine independently reduced small bowel transit (P = 0.0006 and 0.006, respectively, by three-way analysis of variance [ANOVA]; GC 4.3 +/- 0.2 control versus 2.2 +/- 0.3 laparotomy versus 3.6 +/- 0.4 morphine), but morphine did not further worsen postoperative transit (GC 2.4 +/- 0.4; P = 0.42). Although salsalate did not alter baseline transit, pretreatment improved postoperative transit (P = 0.0002; GC 3.6 +/- 0.4). This effect was lost with the addition of morphine (GC 2.7 +/- 0.2; P = 0.21). The MMCs returned earlier after laparotomy in salsalate-pretreated rats (63 +/- 18 minutes salsalate versus 160 +/- 12 minutes laparotomy; P < 0.01, one-way ANOVA). However, this effect was also lost in animals receiving morphine (106 +/- 16 min; P > 0.05). CONCLUSION: Salsalate improves postoperative small bowel motility in a rodent model; however, this effect is masked by morphine.

Animals↗

PubMed1985

Duodenal ulcerogens cysteamine and propionitrile induce gastroduodenal motility alterations in the rat.

The effects of the duodenal ulcerogens cysteamine and propionitrile on gastroduodenal myoelectric activity and intraluminal pressure in the fasted rat as well as on contractility of isolated gut muscle strips were investigated. Duodenal ulcerogens, unlike the nonulcerogen but toxic analogue ethanolamine, caused an early disruption of the myoelectric migrating complex, a marked increase in the spiking activity, and a decrease in the frequency of the slow waves in the duodenum. Both the increased spiking activity and the decreased slow wave frequency were dose dependent for cysteamine. Manometrically recorded contractions at the stomach corpus, midantrum, and antropyloric region as well as in the proximal duodenum of the conscious rat showed decreased contractions at the corpus and midantrum and an increase at the pyloric and duodenal sites during an intravenous infusion of cysteamine. In vitro studies demonstrated that circularly or longitudinally cut muscle strips taken from different regions of the stomach and duodenum responded to cysteamine with increased contractility. In summary, the duodenal ulcerogens cysteamine and propionitrile rapidly induce motor abnormalities in the stomach and duodenum of the rat. In vitro studies suggest that a cholinergic mechanism may be involved. It is possible that motor changes play a role in the pathogenesis of the experimentally induced duodenal ulcers.

Acetylcholine↗

PubMed1987

Valosin stimulates gastric and exocrine pancreatic secretion and inhibits fasting small intestinal myoelectric activity in the dog.

Valosin, a novel 25-amino acid gastrointestinal peptide with N-terminal valine and C-terminal tyrosine, has recently been isolated from porcine upper gut extracts. Its physiologic role is unknown and it does not belong to one of the structurally related gut peptide families. Assuming that valosin may influence gastrointestinal functions, we investigated the effect of high-performance liquid chromatography-pure valosin on gastric and exocrine pancreatic secretion and on the intestinal myoelectric activity in conscious dogs. Intravenous injection of valosin (0.125-1 microgram/kg) dose-dependently increased gastric acid secretion 80-fold over basal, corresponding to 18% of the maximal pentagastrin-induced effect. Pepsin output increased 10-fold over basal (30% of the pentagastrin-stimulated secretion). Half-maximal stimulation by pentagastrin could be further increased dose-dependently by simultaneous administration of valosin. Pancreatic bicarbonate secretion was stimulated 11-fold over basal at 1.0 microgram/kg, reaching about 6% of the secretin-induced maximal output, whereas protein secretion increased 12-fold over basal, corresponding to about 55% of the cholecystokinin-induced maximal output. In fasted dogs, spontaneously occurring migrating myoelectric complexes were substantially delayed during infusion of valosin at a dose of 0.2 microgram/kg. These experiments indicate that valosin may represent a novel member of the regulatory gastrointestinal peptides.

Animals↗

PubMed1999

Evolution of acute cytomegalovirus gastritis to chronic gastrointestinal dysmotility in a nonimmunocompromised adult.

A 30-year-old nonimmunocompromised woman developed chronic gastrointestinal dysmotility as a consequence of acute cytomegalovirus infection. The acute nature of the infection was documented by high immunoglobulin M antibody titer to cytomegalovirus (CMV); the chronicity of the infection was shown by persistence of CMV in biopsy specimens of her gastrointestinal tract over a 21/2-year period. Gastrointestinal dysmotility was confirmed by delayed emptying on gastric nuclear scintigraphy, by retrograde propagation of migrating myoelectric complexes on small intestinal manometry, and by presence of tachygastria on cutaneous electrogastrography. The patient's nausea, vomiting, abdominal pain, and early satiety resolved after a short course of treatment with leuprolide acetate but returned after medication was discontinued. Her symptoms persisted despite clearance of CMV from the gastrointestinal tract after a course of treatment with ganciclovir. These observations show that acute CMV infection can cause gastrointestinal dysmotility in nonimmunocompromised individuals and that the disturbance in gastrointestinal motor function may persist for years after viral infection of the gastrointestinal tract has been eradicated.

Acute Disease↗

PubMed2002

Glucagon-like peptide-1 analogue LY315902: effect on intestinal motility and release of insulin and somatostatin.

LY315902 is an analogue of GLP-1 that yields a reduced clearance and longer half-life. The aim of the study is to assess the effect of LY315902 on fasting gastrointestinal motility, somatostatin and insulin release. Sprague-Dawley rats were fitted with three bipolar electrodes, 15, 25 and 35 cm distal to the pylorus. The effect of LY315902 and GLP-1 on migrating myoelectric complex (MMC) cycle length, duration and propagating velocity of activity fronts was studied for 60 min in conscious animals. The effect of LY315902 and GLP-1 on fasting small bowel motility was dose-dependent and treatment with exendin (9-39)amide, a GLP-1 receptor antagonist, together with LY315902 and GLP-1 completely antagonised the inhibitory effect of LY315902 and GLP-1 on fasting small bowel motility. Pretreatment with the nitric oxide (NO) synthase inhibitor N(omega)-nitro-L-arginine (L-NNA) partly blocked the action of both LY315902 and GLP-1. Plasma insulin concentrations were not different from controls during infusion of LY315902 or GLP-1, while somatostatin concentrations were significantly higher during LY315902 and GLP-1 compared to saline. LY315902 has a longer duration of inhibitory action on the MMC than GLP-1, albeit similar effects on plasma insulin and somatostatin concentrations. The effect of LY315902 on motor control is mediated through the GLP-1 receptor and seems partly dependent on the L-arginine/NO pathway.

Animals↗