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At least 19 recordsLinked to original sources
PubMed1984

Comparative study of pA2 values of pirenzepine and atropine for guinea-pig gastric fundus and gastric smooth muscle.

Concentration-response curves of bethanechol were obtained from isolated guinea pig gastric fundus and gastric circular smooth muscle strips before and after exposure to pirenzepine or atropine. In the presence of pirenzepine and atropine these curves were shifted parallel to the right with no change in maximum response. Against bethanechol, mean pA2 values were 7.06 for pirenzepine and 8.16 for atropine on gastric fundus, with slopes of Schild plots close to unity for both antagonists, whereas in the case of gastric smooth muscle pA2 values were 6.52 for pirenzepine and 8.52 for atropine, with the slope of the Schild plot significantly less than -1 in the case of pirenzepine. The values of the Schild slope seem to indicate that pirenzepine interacts with a single, apparently homogeneous population of muscarinic receptors on gastric mucosa, at variance with the behaviour of pirenzepine on receptors of gastric smooth muscle.

Animals↗
PubMed1986

Motility of isolated mammalian gastric fundus.

Gastric fundus strips (GFS) of rats, guinea-pigs, rabbits, cats and humans, but not of dogs, show spontaneous phasic contractions in vitro. Rabbit, cat, dog and human GFS exhibit dose-dependent responses to acetylcholine (ACh), histamine (His), serotonin (5-HT) and KCl. Guinea-pig drug-induced responses are not dose-dependent. Rat GFS does not respond to His. ED50S for KCl are always higher than for other agonists. ED50S for 5-HT are lower than for other drugs in rats and cats, but not different in other species. Maximal GFS contractions induced by ACh are usually higher than those induced by other drugs.

Acetylcholine↗
PubMed1977

Ultrastructural and carbohydrate histochemical studies on the differentiation and renewal of mucous cells in the rat gastric fundus.

Gastric surface mucous cells (SMC), mucous neck cells (MNC) and their undifferentiated and immature precursors were studied by light and electron microscopic histochemistry. The secretory granules of SMC were smaller, more electron dense and more reactive to PAS and its analogues than those of MNC. Alcian blue demonstrated that the mucus of SMC was acidic and that of MNC was neutral. The periodic acid-thiocarbohydrazide-silver proteinate method revealed the pressence of carbohydrates in the golgi apparatus, condensing vacuoles, secretory granules, apical vesicles and tubules and cell coat. Maturation of SMC during their migration towards the free surface was reflected by an increase in size and number of secretory granules, an increase of RER and microfilaments, and a decrease of microvilli and apical vesicles and tubules. The secretory granules of older SMC were less acidic and possessed a proteinaceous core. Most MNC were fully differentiated, but some immature MNC containing only a few granules were found. Furthermore, undifferentiated cells and intermediates between SMC and MNC were also observed. The presence of both transitional and intermediate forms indicates that both SMC, and MNC arise from the same population of undifferentiated cells. Incorporation of 3H-thymidine revealed that undifferentiated cells, use isthmic SMC, MNC and intermediate cells are proliferative. No proliferative activity was found in foveolar SMC, parietal, chief, fibrillovesicular or endocrine cells.

Animals↗
PubMed1999

Role of nitric oxide in fasting gastric fundus tone and in 5-HT1 receptor-mediated relaxation of gastric fundus.

Fasting gastric fundus tone is maintained by continuous cholinergic input. 5-Hydroxytryptamine-1 (5-HT1) receptor activation decreases gastric fundus tone in humans. Whether this fundus-relaxing effect is mediated via inhibition of cholinergic input or via activation of a nitrergic pathway is unknown. The aim of the present study was to determine the effect of nitrergic inhibition on feline gastric fundus tone and on 5-HT1 receptor-mediated relaxation of the fundus. Administration of Nomega-nitro-L-arginine methyl ester (L-NAME) alone caused a significant decrease of the mean baseline volume (P < 0.005), which was restored completely by addition of L-arginine. Sumatriptan caused a dose-dependent relaxation of the gastric fundus (P < 0.0005). This relaxation was inhibited by L-NAME (P < 0.02) and was restored by prior administration of L-arginine. Buspirone did not cause any change in mean baseline volume, whereas the sumatriptan-induced relaxation was not affected by prior administration of NAN-190. Our data indicate that fasting fundus tone relies not only on continuous cholinergic input but also on continuous nitrergic input, implying that fasting fundus tone is maintained by the balance of a cholinergic and nitrergic drive. Furthermore, fundus relaxation via 5-HT1 receptor activation is mediated through activation of a nitrergic pathway.

Animals↗
PubMed2002

A putative role for S-nitrosoglutathione as the source of nitric oxide in photorelaxation of the mouse gastric fundus.

Mouse gastric fundus strips were relaxed by ultraviolet light (UV) irradiation, exogenous nitric oxide (NO), isoproterenol, S-nitrosoglutathione, S-nitroso-L-cysteine and S-nitroso-N-acetyl-penicillamine. Glutathione did not affect relaxations in response to UV irradiation, exogenous NO and isoproterenol while inhibiting that with S-nitrosoglutathione. L-Cysteine inhibited responses to UV irradiation and exogenous NO, but not in the presence of exogenous Cu(2+)/Zn(2+) superoxide dismutase. However, L-cysteine alone or in combination with Cu(2+)/Zn(2+) superoxide dismutase did not affect the relaxations in response to S-nitroso-L-cysteine. Ethacrynic acid and diamide inhibited photorelaxations but not the relaxations with exogenous NO and isoproterenol. This inhibition was prevented by glutathione, but not by L-cysteine. S-nitrosoglutathione-induced relaxations were abolished by diamide and ethacrynic acid, whereas responses to S-nitroso-L-cysteine and S-nitroso-N-acetyl-penicillamine were only inhibited by ethacrynic acid. These results suggest that S-nitrosoglutathione may, at least in part, be the putative S-nitrosothiol, which is converted to NO in response to UV irradiation in mouse gastric fundus strips.

Acetylcysteine↗
PubMed1983

Volume accommodation by distension of gastric fundus (rabbit) and gastric corpus (cat).

In attempts to identify the structures of the proximal stomach responsible for volume accommodation, the dimensions of a herbivore (rabbit) were compared to those of a carnivore (cat) stomach at various degrees of filling. The total gastric surface area was similar in both species, but the proximal stomach of cats consisted primarily of the segment between the incisura angularis and the cardia (gastric corpus), while the proximal stomach of the rabbit was represented largely by the true fundus (segment orad to cardia). In both species, the muscle coat of the proximal stomach was thinner than that of the distal stomach, but this difference was more prominent in rabbits than in cats. In both species, the length and the angulation of the lesser curvature were little affected by filling of the stomach. Most length increases of the greater curvature occurred proximal to the cardia in the rabbit and proximal to the incisura angularis in the cat. Filling the stomach increased the length of the gastric circumference more steeply in the cat than in the rabbit. In both species, the stomachs shortened in their longitudinal axis in response to a drug that excites gastric smooth muscle (carbachol). A drug that inhibits gastric smooth muscle (isoproterenol) gave the stomach a more elongated shape. Cat stomachs ruptured at higher volumes and intragastric pressures than rabbit stomachs. In the cat, volume accommodation takes place in the transverse axis of the stomach, and parallel to the circular muscle fibers of the gastric corpus. In the rabbit, volume unfolds the gastric fundus in the longitudinal and transverse axes in parallel to the radiating course of the oblique muscle fibers.

Animals↗
PubMed1987

[Gastric fundus necrosis following acute gastric dilatation].

Total gastrectomy with immediate re-establishment of digestive continuity successfully treated a patient with gastric fundus necrosis due to acute dilatation of stomach. The very particular circumstances of onset of this major complication are outlined, diagnosis being dependent on radiological and endoscopic findings. In cases with necrosis of the fundus the extensive nature of the ischemic lesions as shown by results of histopathology strongly suggests the need for total gastrectomy in these patients.

Bulimia↗
PubMed2002

Investigation of the potential modulatory effect of biliverdin, carbon monoxide and bilirubin on nitrergic neurotransmission in the pig gastric fundus.

In porcine gastric fundus, we have investigated the colocalization of the bile pigment biosynthetic enzymes heme oxygenase-2 and biliverdin reductase with neuronal nitric oxide synthase (nNOS), the effect of carbon monoxide (CO) on fundic circular smooth muscle and the possible modulatory effect of the bile pigments biliverdin and bilirubin on CO-mediated relaxations and on nitrergic relaxation. Heme oxygenase-2 and biliverdin reductase immunoreactivity was present in all nNOS containing myenteric neurons. CO induced a concentration-dependent relaxation of fundic circular smooth muscle strips, which was completely blocked by the specific guanylate cyclase inhibitor 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one (ODQ). 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (YC-1), biliverdin and bilirubin strongly enhanced the amplitude of the CO-induced relaxation. Tin protoporphyrin had no effect on electrically induced nitrergic relaxation, but spectrophotometric analysis learned that incubation of porcine gastric fundus circular muscle strips with tin protoporphyrin did not influence heme oxygenase activity. In conclusion, our data suggest that nitrergic neurons in the pig gastric fundus are able to produce biliverdin and bilirubin, and that these agents potentiate the relaxant effect of CO, which is formed concomitantly with biliverdin by heme oxygenase-2.

Animals↗
PubMed2000

Influence of sumatriptan on gastric fundus tone and on the perception of gastric distension in man.

BACKGROUND: In animals, activation of 5-HT(1) like receptors causes a relaxation of the gastric fundus through the activation of intrinsic inhibitory neurones. AIMS: To investigate the effect of sumatriptan, an agonist at enteric neuronal 5-HT(1) receptors, on fasting fundus tone and sensitivity to gastric distension in man. METHODS: A gastric barostat was used to study the effect of placebo and sumatriptan, 6 mg subcutaneously, on basal fundic tone in healthy subjects. In addition, stepwise isobaric and isovolumetric gastric distensions were performed and perception was measured before and after the administration of placebo and sumatriptan. RESULTS: Placebo had no significant effects on gastric tone and on perception. Sumatriptan induced an immediate relaxation of the gastric fundus, reflected by an intragastric volume increase of 209 (39) ml (p<0.0005). After sumatriptan, intragastric pressures at the thresholds for perception or discomfort were not significantly altered. However, the intragastric volumes and the corresponding calculated wall tensions at perception and discomfort thresholds were significantly increased. CONCLUSIONS: Administration of the 5-HT(1) receptor agonist sumatriptan induces a relaxation of the gastric fundus in man, allowing larger intragastric volumes before thresholds for perception or discomfort are reached. The effects of sumatriptan on the gastric fundus may have therapeutic potential in the treatment of patients with functional dyspepsia.

Adult↗
PubMed1990

Relaxant effects of alpha-adrenoceptor agonists in the rat isolated gastric fundus.

In rat gastric fundus preparations with tone raised by the addition of barium chloride or carbachol, and in the presence of propranolol (2 microM) to prevent beta-adrenoceptor mediated effects, the adrenoceptor agonists noradrenaline, adrenaline, alpha-methylnoradrenaline, isoprenaline, cirazoline and phenylephrine all caused concentration-related relaxant responses. Relaxations to the catecholamines were poorly antagonized by prazosin (0.01-1 microM) resulting in the slopes of Schild plots being less than unity, low pA2 values for prazosin against the catecholamines and a clear relaxant effect of the catecholamines even in the presence of 1 microM prazosin. The prazosin-resistant relaxations were unaffected by higher concentrations of prazosin (2 microM) and propranolol (30 microM) or by further additions of idazoxan (1 microM) or haloperidol (30 microM). The relaxations were not due to a non-specific effect of the catechol nucleus since neither dihydroxyphenylethylene glycol (DOPEG) nor dihydroxyphenylacetic acid (DOPAC) produced relaxant effects at concentrations up to 300 microM. In contrast to the results with the catecholamines, prazosin was a potent antagonist of the relaxant effect of cirazoline and phenylephrine, although the antagonism was difficult to quantify due to a lowering of the slope of the concentration response curves to cirazoline and phenylephrine with the higher concentrations of prazosin (0.1 and 1.0 microM). In conclusion postjunctional relaxatory effects of catecholamines in the rat gastric fundus are mediated partly via alpha 1-adrenoceptors and partly via an atypical adrenoceptor.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

Is peptide histidine isoleucine an inhibitory nonadrenergic noncholinergic neurotransmitter in the rat gastric fundus?

In the rat gastric fundus, vasoactive intestinal polypeptide (VIP) contributes to the nonadrenergic noncholinergic (NANC) inhibitory neurotransmission and coexists with its related peptide, peptide histidine isoleucine (PHI). As the two neuropeptides are co-released and have similar actions in different biological systems, the effect of PHI in the rat gastric fundus was studied in order to investigate whether it might be a co-transmitter of VIP in the inhibitory NANC neurotransmission in this tissue. Auxotonic responses were measured in longitudinal muscle strips from the gastric fundus of reserpinized rats (5 mg/kg i.p., 24 hr before sacrifice), suspended between parallel platinum electrodes in Krebs solution containing atropine (1 microM) and 5-hydroxytryptamine (3 microM). PHI induced concentration-dependent relaxations (10 nM-1 microM), qualitatively similar to those induced by electrical field stimulation (1 msec, supramaximal voltage, 0.25-16 Hz) and by VIP (0.3-100 nM), although PHI was about 30 times less potent than VIP. The submaximal relaxation induced by PHI (100 nM) was not influenced by tetrodotoxin (1 microM), hexamethonium (500 microM) and propranolol (10 microM) plus phentolamine (3 microM). Incubation during 60 min with a specific PHI-antiserum completely prevented the relaxation induced by PHI (100 nM) and reduced by 26% that induced by electrical field stimulation at 1 Hz; the procedure had no influence on the relaxation induced by VIP (3 nM) or isopropylnoradrenaline (10 nM). Incubation during 60 min with a specific VIP-antiserum completely prevented the relaxation induced by VIP (3 nM) and halved the relaxatory response to electrical field stimulation at 1 Hz, while it had no influence on the relaxation induced by PHI (100 nM) or isopropylnoradrenaline (10 nM). Control serum had no influence on any of the relaxant stimuli. In conclusion, PHI mimics the electrically induced NANC relaxation in the rat gastric fundus; its action is located at muscle level and does not involve alpha-, beta- or nicotinic receptors. The results obtained in the presence of the antisera provide further confirmation that VIP contributes to the NANC inhibitory neurotransmission of the rat gastric fundus and leave open the possibility that PHI is involved as co-transmitter.

Animals↗
PubMed2000

Evidence that adenosine 5'-triphosphate is the third inhibitory non-adrenergic non-cholinergic neurotransmitter in the rat gastric fundus.

In the rat gastric fundus, non-adrenergic, non-cholinergic (NANC) relaxations are mediated by nitric oxide (NO), vasoactive intestinal polypeptide (VIP), and a third, as yet unidentified, neurotransmitter. The possible involvement of adenosine 5'-triphosphate (ATP) in the NANC relaxations was examined using pyridoxalphosphate-6-azophenyl-2',5'-disulphonic acid (PPADS), apamin and desensitization to alpha,beta-methylene ATP. NANC responses were studied in the absence and presence of N(G)-nitro-L-arginine methyl ester (NAME; 100 microM) and alpha-chymotrypsin (1 u ml(-1)), to inhibit responses to NO and VIP, respectively. PPADS (100 microM), apamin (1 microM) and desensitization to alpha,beta-methylene ATP (10 microM, three additions) all significantly (P<0.05) reduced NANC relaxations to electrical field stimulation (0.5 - 4 Hz, 30 s trains) in longitudinal strips of rat gastric fundus and almost abolished the residual relaxation remaining in the presence of NAME and alpha-chymotrypsin. PPADS had no effect on responses to the NO-donor, sodium nitroprusside (SNP), or VIP. Apamin slightly reduced relaxations to SNP, but did not affect those to VIP, whereas desensitization to alpha,beta-methylene ATP markedly reduced responses to both SNP and VIP. The effects of PPADS and apamin in this study provide strong evidence that the third inhibitory NANC neurotransmitter in the rat gastric fundus is ATP.

Adenosine Triphosphate↗
PubMed1981

Is glucagon present in the human gastric fundus?

The presence of pancreatic type glucagon in the fetal and adult human gastric fundus was examined by radioimmunoassay and by an indirect immunofluorescence technique using specific antiserum against pancreatic glucagon. Although pancreatic type glucagon-containing cell (glucagon-positive cell) were demonstrated in the fetal gastric fundus in 16th, 18th, 23rd and 29th week's gestation, they were not detected in the adult gastric fundus. This immunohistochemical finding was supported by radioimmunoassay study for glucagon in gastric fundus in which there was 52 pg/mg of glucagon in the fetal gastric fundus at 20th week's gestation while glucagon was negligible in the adult gastric fundus. The findings, therefore, suggest that glucagon-positive cells in the human gastric fundus may play an important role in the maintenance of fetal life. Moreover, one fourth of glucagon-positive cells in the fetal gastric fundus reached the gut lumen with their cytoplasmic processes. In view of the finding that none of the canine glucagon-positive cells in the gastric fundus had contact with the gut lumen, the morphological feature of glucagon-positive cells in the human, fetal gastric fundus suggests that the function of glucagon-positive cells in the human, fetal gastric fundus may be somewhat different from that in other mammals.

Adult↗
PubMed1998

The role of a ryanodine-sensitive Ca(2+)-store in the regulation of smooth muscle tone of the cat gastric fundus.

The smooth muscle of the gastric fundus maintains spontaneous tone, but the mechanism underlying this activity is not fully understood. The aim of the present study was to examine whether Ca2+ release from the sarcoplasmic reticulum (SR) could play a role in the maintenance of the spontaneous smooth muscle tone of the cat gastric fundus. The effects on the contractile activity of SR Ca2+ release activators ryanodine and caffeine and of the inhibitor ruthenium red were studied. The contractile activity of isolated muscle strips was recorded under isometric conditions using organ baths. Ryanodine concentration-dependently (10(-7)-3.10(-5) mol/l) increased the tone of the fundus strips. In the presence of nifedipine (10(-5) mol/l), ryanodine induced a nifedipine-resistant tonic contraction. The tonic contraction induced after inhibition of the SR Ca(2+)-pump by cyclopiazonic acid was potentiated by ryanodine (10(-5) mol/l). In strips precontracted with supramaximal concentration of acetylcholine (10(-5) mol/l), ryanodine (3.10(-5) mol/l) further potentiated the tone. Caffeine (10(-4)-10(-2) mol/l) decreased and even completely inhibited the tone, suggesting some other effects of caffeine. Ruthenium red concentration-dependently (10(-6)-10(-4) mol/l) decreased the tone. The present data provide evidence for the role of Ca2+ release from a SR ryanodine-sensitive Ca2+ store in the maintenance of the muscle tone of the cat gastric fundus.

Animals↗