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PubMed1999

Regulatory effect and mechanism of gastrin and its antagonists on colorectal carcinoma.

AIM:To explore the effect and mechanism of gastrin and its antagonists prog lumide and somatostatin on colorectal carcinoma and their clinical significance.METHODS:A model of transplanted human colonic carcinoma was established from SW480 cell line in gymnomouse body.The volume and weight of transplanted carcinoma was observed under the effect of pentagatrin (PG), proglumide (PGL) and octapeptide somotostatin (SMS201-995, SMS). The cAMP content of carcinoma cell was determined by radioimmunoassay and the DNA, protein content and cell cycle were determined by flow-cytometry. The amount of viable cells was determined by MTT colorimetric analysis,IP(3) content was determined by radioimmunoassay, Ca(2+) concentration in cell by fluorometry and PKC activity by isotopic enzymolysis. The expression of gastrin, c-myc, c-fos and rasP21 in 48 cases of colorectal carcinoma tissue was detected by the immuno-cytochemistry SP method. Argyrophilia nucleolar organizer regions was determined with argyrophilia stain.RESULTS:The volume,weight, cAMP, DNA and protein content in carcinoma cell, cell amount and proliferation index of S and G(2)M phase in PG group were all significantly higher than those of control group. When PG was at the concentration of 25mg/L, the amount of viable cells, IP(3) content and Ca(2+) concentration in cell and membrane PKC activity in PG group were significantly higher than those in control group; when PGL was at a concentration of 32mg/L, they dropped to the lowest level in PG (25mg/L)+PGL group, but without significant difference from the control group. The positive expression rate of gastrin, c-myc, c-fos and rasP21 in carcinoma tissue was 39.6%, 54.2%, 47.9% and 54.2% respectively and significantly higher than that in mucosa 3cm and 6cm adjacent to carcinoma tissue and normal colorectal mucosa. The positive expression rate of gastrin of highly differentiated adenocarcinoma group was significantly higher than that of poorly differentiated and mucinous adenocar-cinoma groups. The AgNORs count of carcinoma tissue was significantly higher than that in mucosa 3cm and 6cm adjacent to carcinoma tissue and normal colorectal mucosa; and the positive expression of c-myc and c-fos and the AgNORs count in gastrin-positive group was significantly higher than those in gastrin negative group.CONCLUSION:Pentagastrin has a promoting effect on the growth of transplanted human colonic carcinoma from SW480 cell line. PGL has no obvious effect on the growth of human colonic carcinoma SW480 cell line, but could inhibit the growth promoting effect of PG on transplanted carcinoma. Somatostatin can not only inhibit the growth of transplanted human colonic carcinoma from SW480 cell line directly but also depress the growth-promoting effect of gastrin on the transplanted carcinoma. Some colorectal carcinoma cells can produce and secrete gastrin through autocrine, highly differentiated adenocarcinoma express the highest level gastrin.Endogenous gastrin can stimulate the cell division and proliferation of carcinoma cell and promote the growth of colorectal carcinoma regulating the expression of oncogene c-myc, c-fos. Our study has provided experimental basis for the adjuvant treatment using gastrin antagonist such as PGL, somatostatin of patients with colorectal carcinoma.

Journal Article↗
PubMed2002

[The placebo effect--a biochemical basis for a psychosomatic phenomenon].

We review the research over the past decade on the subject of the Placebo Neurochemical mechanism, and it's random presence in the clinic. Our goal is to present the scientific basis of the placebo, and to arouse the awareness of physicians and scientists to the crucial role of placebo in medicine and pharmacological research. The modeling of rationality in modern times displaced the placebo issue to the sidelines of consensus, and it was only around 1950 that scientific interest in the phenomenon reawakened. Today the existence of a Placebo Effect is not doubted--not in everyone, and not at all times, but it's existence is not doubted in relation to groups of people throughout their lives. The involvement of a neurochemical mechanism in the Placebo Effect is also supported by the literature presented, and chemicals such as CCK, Naloxone, Proglumide, and Endorphins seem to effect the neuronal webs mediating the Analgestic Placebo Effect.

Analgesics↗
PubMed2002

Effects of cholecystokinin octapeptide on rat cardiac function and the receptor mechanism.

The aim of this study was to explore the effects of cholecystokinin octapeptide (CCK-8) on cardiac function and the receptor mechanism in anesthetized rats. The mean arterial pressure (MAP), heart rate (HR), the left ventricle systolic pressure (LVP) and the maximal/minimum rate of LVP (+/-LV dp/dt(max)) were measured. The results obtained are as follows. (1) Low dose of CCK-8 (0. 4 microgram/kg i.v.) caused tachycardia and slight increase in MAP, LVP and LV dp/dt(max) (P<0.01), while medium dose (4.0 microgram/kg i.v.) and high dose of CCK-8 (40 microgram/kg i.v.) elicited a bradycardia and marked increase in MAP, LVP and LV dp/dtmax (P<0.01). (2) Proglumide (1.0 mg/kg i.v.), a CCK-receptor (CCK-R) antagonist, significantly inhibited the pressor effects of CCK-8, whilst it reversed the bradycardic responses (P<0.01). (3) Using reverse transcription polymerase chain reaction (RT-PCR), CCK-A receptor (CCK-AR) and CCK-B receptor (CCK-BR) mRNA were expressed in myocardium of rats. The above results indicate that CCK-8 may enhance cardiac function in a dose-dependent manner and elicit a change in HR, which is likely induced by the activation of CCK-R on myocardium.

Animals↗
PubMed2004

Cholecystokinin octapeptide increases free intracellular calcium of guinea pig cardiomyocytes through activation of Ca2+ channel and tyrosine kinase.

The aim of the present study was to explore the effect of cholecystokinin octapeptide (CCK-8) on [Ca(2+)](i) and its signal transduction mechanism in isolated guinea pig cardiomyocytes. [Ca(2+)](i) was measured by laser scanning confocal microscopy in single ventricular myocytes which were dissociated by enzymatic dissociation method and loaded with Fluo 3-AM. The changes in [Ca(2+)](i) were represented by fluorescent intensity (F(i)) or relative fluorescent intensity (F(i)/F(O)%). The results obtained are as follows. (1) In the normal Tyrode's solution containing 1.0 mmol/ L Ca(2+), CCK-8 (1-10(4) pmol/L) elicited a rapid and marked increase in [Ca(2+)](i). (2) When cardiomyocytes were pretreated with the Ca(2+) chelator EGTA (3 mmol/L) and Ca(2+) channel antagonist nisoldipine (0.5 micromol/L) for 5 min, CCK-8 (10(2)pmol/L) caused a slow and small increase in [Ca(2+)](i) (p< 0.01). (3) Pretreatment with the nonselected CCK- receptor (CCK-R) antagonist proglumide (6 micromol/L) or the tyrosine kinase inhibitor genistein (1 micromol/L) for 5 min could inhibit the increase of [Ca(2+)](i) induced by CCK-8 (10(2) pmol/L) (p<0.01). The results suggest that CCK-8 increases the [Ca(2+)](i) via activating the receptor-operated Ca(2+) channel and eliciting the influx of Ca(2+) in isolated guinea pig cardiomyocytes, in which tyrosine kinase may be involved.

Animals↗
PubMed1992

Cholecystokinin type A and type B receptor antagonists produce opposing effects on cholecystokinin-stimulated beta-endorphin secretion from the rat pituitary.

Cholecystokinin octapeptide (CCK-8) is a potent corticotroph secretagogue. Consistent with earlier reports, the present results demonstrate that CCK-8 administration to rats elevates circulating beta-endorphin and adrenocorticotropin, but not alpha-melanocyte-stimulating hormone concentrations. This response was blocked by dexamethasone pretreatment, but not by vagotomy, and it could not be reproduced by i.c.v. CCK-8 injection, evidence that CCK-8 exerts its effects by directly activating cholecystokinin (CCK) receptors localized on anterior pituitary corticotrophs rather than in brain or the vagus nerve. Subsequent experiments demonstrated further that type A CCK receptors primarily mediate the stimulatory effect of CCK-8 on corticotroph secretion. Thus, devazepide, a selective CCK-A receptor antagonist, produced a dose-related inhibition of the CCK-8-stimulated rise in circulating beta-endorphin concentrations. Less selective CCK-A antagonists, including proglumide and lorglumide, produced little or no effect, however. Unexpectedly, the CCK-B receptor antagonist, L-365,260, enhanced the response to CCK-8, an effect diametrically opposite to that produced by CCK-A antagonists. These observations indicate that CCK-A and CCK-B receptors mediate quite different, if not opposing, roles in regulating corticotroph secretion.

Animals↗
PubMed1986

Cholecystokinin-8 stimulates adrenocorticotropin release from anterior pituitary cells.

Cholecystokinin octapeptide (CCK-8) stimulated adrenocorticotropin hormone (ACTH) release from both rat anterior pituitary cells in culture and a tumor cell line of the mouse anterior pituitary (AtT-20/D16-16). The stimulation of ACTH release was dependent on the time of exposure to CCK-8 and the concentration of this peptide applied to anterior pituitary cells. Cerulein evoked ACTH release whereas human gastrin 1, CCK-4 and desulfated CCK-8 only produced minimal affects on ACTH release at concentrations of 10(-4) M. In contrast, these latter three peptides were as effective as CCK-8 in inducing the secretion of amylase from pancreatic acinar cells. Antagonists of CCK-8 receptors in the pancreas such as proglumide, benzotript and dibutyryl cyclic GMP did not affect the ACTH release response to CCK-8. The CCK-8 stimulation of ACTH release was calcium-dependent and blocked by glucocorticoid pretreatment. The mechanisms by which CCK-8 evoked ACTH release appears distinct from that of other ACTH secretagogues such as corticotropin releasing factor and vasopressin. The data suggest that CCK-8 is a corticotropin releasing factor-like agent acting through a putative novel receptor subtype in the anterior pituitary.

Adrenocorticotropic Hormone↗
PubMed1989

Biological basis of omeprazole therapy.

There are two means of reducing acid secretion. The best studied is inhibition of stimulation of the parietal cell. There are three major types of receptors that activate secretion by this cell and two classes of receptor antagonists, as well as at least two intracellular messenger pathways. The receptors are for histamine (H2 subtype), acetyl choline (M2 subtype) and gastrin. Antagonists of these receptors include the H2-antagonist class (Tagamet, Zantac and Pepcid), the M1 muscarinic antagonists (pirenzepine, telenzepine) and the gastrin antagonist, proglumide. The major pathway for stimulation appears to be the H2-receptor, since this is the only receptor that stimulates adenylate cyclase, and both acetyl choline and gastrin release histamine locally within the gastric mucosa. However, these agonists elevate intracellular calcium, which has a partially independent action on acid secretion. Accordingly, the most efficacious type of receptor antagonist will be of the H2 class, which is borne out by clinical experience. Prostaglandins of the E type prevent adenylate cyclase stimulation by histamine and are also effective antisecretory agents. It will be difficult to abolish acid secretion entirely by a single receptor antagonist, although longer-acting H2-antagonists should show clinical superiority to short-acting antagonists of this type. An alternative approach to acid suppression is to block the terminal step of acid secretion, the gastric proton pump (H+, K(+)-ATPase). This enzyme is virtually unique to the parietal cell and, when active, forms a very acidic space within the parietal cell called the secretory canaliculus. Activation of acid secretion involves several steps. The enzyme is present in cytosolic membranes when the cell is at rest and moves to the membrane of the secretory canaliculus when stimulated. Simultaneously, there is an increased permeability of potassium chloride (KCl), which allows presentation of K+ to the luminal surface of the pump and H+ for K+ exchange. The result is the secretion of HCl into the canaliculus, and hence into the gland lumen and then the stomach. There are two classes of pump inhibitors. One class is K+ competitive and relatively selective for the H+, K(+)-ATPase, as exemplified by SCH28080. This class has not yet been used in man. The other class is specific to the functioning H+, K(+)-ATPase in the stomach. It is exemplified by omeprazole (Losec). This compound is a weak base with a pKa of 4. In the unprotonated, uncharged form it will penetrate cell membranes and, at pH less than 4, it becomes protonated and therefore charged.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphatases↗
PubMed1989

[Antagonism of morphine analgesia and electroacupuncture analgesia by cholecystokinin octapeptide (CCK-8) administered in periaqueductal gray (PAG) of the rabbits].

We have reported that intracerebroventricular (i. c. v.) injection of 1-4 ng of CCK-8 to the rat produced a remarkable antagonistic effect on morphine analgesia. In order to study the species specificity and the site of action, CCK-8 was microinjected into the PAG of the rabbit, and its influence on morphine analgesia and electroacupuncture analgesia was observed. The latency of the escape response (ERL) to radiant heat focused on the snout was measured as an index of the pain threshold. Microinjections were made via cannulae chronically implanted into the PAG. The drug solutions were delivered in a volume of 1 microliter, at a speed of 0.125 microliter/min. The ERL was measured for a period of 60 or 70 minutes at 10 min intervals. 1. CCK-8 administered unilaterally to the PAG of the rabbit at a dose of 3 ng antagonized the analgesia induced by morphine (4 mg/kg, i. v.) by 73% (P less than 0.001), and reduced the analgesic effect of electroacupuncture by 67% (P less than 0.001). These effects were dose-dependent within the range from 1.5 ng to 6.0 ng. The effect of CCK-8 was reversed by CCK receptor blocker proglumide (4 microliters, intra-PAG injection). Unsulfated CCK-8 (CCK-us) had no effect in this regard. These results indicate that in the PAG of the rabbit, exogenously administered CCK-8 was capable of antagonizing opioid analgesia by the activation of CCK receptors. 2. Two groups of rabbits were given with morphine (2 mg/kg, i. v.) and simultaneous injection of CCK-8 antiserum (CCK-AS, 1 microliter) or normal rabbit serum (NRS) into the PAG.(ABSTRACT TRUNCATED AT 250 WORDS)

Acupuncture Analgesia↗
PubMed1985

Characterization of cholecystokinin receptor sites in guinea-pig cortical membranes using [125I]Bolton Hunter-cholecystokinin octapeptide.

[125I]Bolton Hunter-cholecystokinin octapeptide (BH-CCK8) has been prepared using a modified method and was used to study putative cholecystokinin (CCK) receptor sites in the guinea-pig cerebral cortex. Specific binding of [125I]BH-CCK8, defined as the difference in binding in the absence and presence of 10(-6) M CCK8, was 70% of total binding. In saturation experiments, the apparent dissociation constant (Kd) was 1 nM and total binding capacity was 28 fmol/mg of protein. In association experiments, conducted at 30 degrees C, binding of [125I]BH-CCIK8 reached equilibrium in approximately 150 min. Binding was stable for 4 hr and was reversed by the addition of unlabeled CCK8-sulfated. Dissociation of bound ligand was biphasic and the apparent T1/2 was 45 min. Analyses of kinetic experiments yielded an association rate constant of 0.58 X 10(8) min-1 M-1 and a dissociation rate constant for the slower component of 0.012 min-1. Dithiothreitol increased and N-ethylmaleimide decreased specific binding of [125I]BH-CCK8, indicating that CCK receptor sites involve sulfhydryl groups. In competition experiments, the potency of CCK4 was enhanced 50-fold with addition of protease inhibitors. The rank order of CCK-related peptides was CCK8-sulfated greater than or equal to Gastrin 17 greater than or equal to CCK33 greater than CCK4 greater than or equal to CCK8-desulfated. Proglumide, a proposed CCK antagonist in the periphery and brain, was inactive at 10(-3) M. The specificity of [125I]BH-CCK8 binding sites are similar to that reported for [125I]BH-CCK33.

Animals↗
PubMed1987

Inhibition of epidermal growth factor binding in rat pancreatic acini by palmitoyl carnitine: evidence for Ca2+ and protein kinase C independent regulation.

D,L-Palmitoyl carnitine (PC), an inhibitor of protein kinase C, decreased [125I]epidermal growth factor (EGF) cell-associated radioactivity in rat pancreatic acini. H-7, another inhibitor of protein kinase C, failed to inhibit [125I]EGF binding. Palmitate, carnitine, acetylcarnitine, and 2-tetradecylglycidic acid methyl ester (a specific inhibitor of endogenous PC formation) did not alter [125I]EGF binding. PC conjugated to bovine serum albumin (PC-BSA) decreased [125I]EGF cell-associated radioactivity to the same extent as PC. Neither compound affected the distribution of cell-associated radioactivity into acid-resistant and acid-dissociable compartments. In contrast, cholecystokinin octapeptide (CCK8) and 12-O-tetradecanoyl-phorbol-13-acetate (TPA) markedly inhibited the distribution of [125I]EGF into the acid-resistant compartment. Proglumide, a competitive antagonist of CCK8, reversed the inhibitory action of CCK8 but not that of PC-BSA. PC-BSA did not inhibit [125I]insulin binding, and did not enhance amylase release, a Ca2+-mediated effect. Further, its inhibitory effect on [125I]EGF cell-associated radioactivity was not additive with the inhibitory effect of the calcium ionophore A23187. Both PC-BSA and H-7 inhibited Ca2+- and phospholipid-dependent kinase activity in soluble and particulate fractions when added to disrupted acini, but in the particulate compartment only when added to intact acini. These findings suggest that PC-BSA may regulate EGF binding via a novel mechanism that is independent of protein kinase C activation or Ca2+ mobilization.

Animals↗
PubMed1986

Cholecystokinin octapeptides alter the release of endogenous dopamine from the rat nucleus accumbens in vitro.

Sulfated cholecystokinin octapeptide (CCK-8S) has been reported to be extensively colocalized with dopamine in the posterior, but not the anterior, portion of the nucleus accumbens (NAc). The hypothesis tested in the present study was that CCK-8S alters the release of dopamine in this structure and the actions it produces are dependent on the extent of colocalization with dopamine. We observed in vitro that CCK-8S enhanced the resting release of dopamine from the posterior, but not anterior, NAc. It was also found that CCK-8S attenuated the release of dopamine induced by potassium-evoked depolarization in both regions of the NAc, although the concentration-release curves for the two areas differed. In the posterior NAc, a biphasic response was seen whereas, in the anterior NAc, there was a monophasic attenuation. Proglumide, a putative CCK-8S antagonist, was found to antagonize the action of a low concentration of CCK-8S on 40 mM K+-induced dopamine release from slices of the posterior, but not anterior, NAc. Unsulfated CCK-8 had mixed action on K+-evoked dopamine release, as it enhanced this form of release in the posterior NAc but attenuated it in the anterior NAc. Additionally, we found no effect of sulpiride on the actions of CCK-8S with respect to evoked release, suggesting that CCK-8S is not acting to alter dopamine autoreceptor function, as has recently been hypothesized. In summary, our results demonstrate that the observed effects of CCK-8S on dopamine release are dependent upon the region of the NAc studied, and there appear to be different subtypes of CCK-8S receptors present in the two regions.

Animals↗
PubMed1985

Cholecystokinin potentiates dopamine-mediated behaviors: evidence for modulation specific to a site of coexistence.

Cholecystokinin coexists with dopamine in mesolimbic neurons in mammalian brain. When injected directly into the nucleus accumbens, cholecystokinin (CCK) potentiated dopamine (DA)-induced hyperlocomotion and apomorphine-induced stereotypy. These effects were not mimicked by nonsulfated CCK, but were blocked by proglumide, a putative CCK antagonist, as well as by antisera raised against sulfated CCK. CCK alone had no effect on locomotion or sterotypy, indicating that this peptide acts primarily as a modulator of DA-mediated behaviors in the mesolimbic pathway. In addition, CCK did not potentiate DA-induced hyperlocomotion or apomorphine-induced stereotypy when injected into the caudate nucleus, where CCK and DA are localized in separate neurons in rats. Facilitation of DA-mediated behaviors by CCK may represent a functional interaction specific to the neuromodulator-neurotransmitter coexistence phenomenon.

Animals↗
PubMed1985

Electrophysiological effects of cholecystokinin: central dopaminergic systems.

The coexisting cholecystokinin (CCK)/dopamine (DA) neurons are located predominantly in the ventral tegmental area of the rat and project to the medial part of the nucleus accumbens (NAc). Iontophoretically applied CCK consistently activated presumed CCK/DA cells as well as those cells receiving CCK/DA projections in the medial NAc. Unsulfated CCK had little or no effect. The putative CCK antagonist proglumide selectively blocked the activation produced by CCK but not glutamate. DA also reversed CCK-induced excitation, presumably by its hyperpolarizing actions. These results suggest that CCK and DA may interact to influence the CCK/DA system.

Animals↗
PubMed1982

Cholinergic and peptidergic receptors on isolated human antral smooth muscle cells.

Smooth muscle cells were isolated from segment so of human antrum obtained at operation. The presence, activity, and specificity of receptors to acetylcholine, the C-terminal octapeptide of cholecystokinin, methionine-enkephalin, and vasoactive intestinal peptide were examined. Muscarinic cholinergic receptors sensitive to low concentrations of atropine, cholecystokinin receptors sensitive to proglumide and dibutyryl cyclic guanosine monophosphate, enkephalin receptors sensitive to naloxone were demonstrated and found to mediate contraction. Vasoactive intestinal peptide receptors were demonstrated also and found to mediate relaxation. The stoichiometry and specificity of responses were closely similar to those previously found in isolated gastric smooth muscle cells of the guinea pig. The existence of high-affinity functional receptors on smooth muscle cells, together with the presence of the peptides in nerve terminals adjacent to these cells, makes it possible for these peptides to act as neurotransmitters.

Cholecystokinin↗
PubMed1984

Possible mechanisms of action of caerulein on intestinal motility of sheep.

The authors report the stimulatory effects provoked by caerulein on caecum and colon motilities in sheep which are quite opposite to those exerted by the same peptide on the forestomach and abomasal sections. By means of various pharmacological tools these effects are suggested to be attributable to a direct effect of caerulein on the smooth muscle of these viscera through the involvement of receptors different from those ones on which CCK may be antagonizable by proglumide or cGMP pretreatments.

Animals↗
PubMed1993

[Effect of KSG-504, a new synthetic cholecystokinin receptor antagonist on ethionine-induced acute pancreatitis in rats].

KSG-504, a new synthetic cholecystokinin (CCK) receptor antagonist derived from proglumide, has superior selectivity and affinity to CCK-A receptors. We have investigated the effect of KSG-504 on ethionine-induced acute pancreatitis in rats and the influence of endogenous CCK on evolution of pancreatitis and regeneration of pancreatic acinar cells. Reduction of pancreatic proteins and digestive enzyme contents was dose-dependently prevented by subcutaneous administration of KSG-504. The inhibition of evolution of pancreatitis was demonstrated histologically in KSG-504 treated rats. The effect of KSG-504 on pancreatic regeneration was evaluated by bromodeoxyuridine labeling index (B.L.I.) of acinar cells. There was no significant difference of B.L.I. between KSG-504 treated and non-treated rats. These results suggest that KSG-504 has a beneficial effect on ethionine-induced acute pancreatitis by blockade of endogenous CCK.

Acute Disease↗
PubMed1996

Potentiation by baclofen of gastric acid secretion stimulated by secretagogues in vagotomized rats under anesthesia.

The effect of intravenous administration of baclofen, a GABA(B) receptor agonist, on gastric acid secretion from perfused stomach was studied in vagotomized rats anesthetized with urethane. Baclofen did not stimulate acid secretion by itself. In contrast, baclofen dose-dependently potentiated acid secretion induced by pentagastrin, bethanechol and direct vagal stimulation, but not by histamine. Baclofen-potentiated acid secretion induced by pentagastrin and bethanechol was not influenced by pretreatment with atropine or cimetidine, respectively. Baclofen-potentiated acid secretion evoked by direct vagal stimulation was prevented by pretreatment with proglumide which is a gastrin receptor antagonist. Baclofen-potentiated acid secretion evoked by bethanechol was partly prevented by bicuculline methiodide which is a GABA(A) receptor antagonist, but not by phaclofen which is a GABA(B) receptor antagonist, suggesting an involvement of peripheral GABA(A) receptors. Baclofen-potentiated acid secretion induced by direct vagal stimulation was not affected by the change of body temperature. These results suggest that baclofen stimulates acid secretion under certain conditions, and that two mechanisms are involved in this effect. The effects of baclofen on acid secretion may be mediated by increasing the release of histamine by pentagastrin, bethanechol and direct vagal stimulation. In addition, baclofen would also be effective if muscarinic agents were already occupying muscarinic acetylcholine receptors on parietal cells.

Anesthesia↗
PubMed1997

[Role of cytosolic calcium release on gastrin induced contraction of gastric muscle cells of rat].

The present study was conducted to investigate the contractile effect of pentagastrin (G5) on isolated smooth muscle cells of rat stomach and role of cytosolic-free calcium ([Ca2+]i) release during contraction of gastric muscle cells induceed by G5. The results were as follows: (1) G5 induces contraction of smooth muscle cells isolated from gastric body, anturm and pylorus, in a dose-dependent manner from 4 x 10(-8) mol/L to 16 x 10(-8) mol/L, with the maximal effectiveness in antrum, (2) The action of G5 can be blocked by proglumide and anti-gastrin serum, but not by atropine. (3) The effect of acetylcholine and G5 are addtive when administrated simultaneously (4) Inhibitor of intracellular Ca2+ release TMB-8 could also suppress the G5 effect. (5) The effect of G5 could be seen accompaning significant increase of intracellular Ca2+ concentration. The above results suggested that the G5 induced contraction of gastric smooth muscle cells of rat is mediated via a distinct, specific type of receptors and cytosolic calcium release.

Animals↗