Interaction of gastrin I, secretin, and cholecystokinin on gallbladder smooth muscle

1976 ◽  
Vol 230 (3) ◽  
pp. 553-556 ◽  
Author(s):  
J Ryan ◽  
S Cohen
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Motor Function ◽  
Muscle Tone ◽  
Dose Range ◽  
Maximum Response ◽  
Maximal Response ◽  
Gallbladder Contraction ◽  
Gallbladder Contractility

The effect of cholecystokinin (CCK), the octapeptide of cholecystokinin (CCK-OP), gastrin I, and secretin was studied on guinea pig gallbladder smooth muscle in vitro. Both CCK and CCK-OP stimulated gallbladder contraction, with CCK-OP being more potent. Gastrin I, over a wide dose range, had no effect on gallbladder contractility. Secretin alone also showed no effect on gallbladder smooth muscle but in combination with CCK-OP it produced a noncompetitive type of inhibition. Michaelis-Menten kinetics showed the calculated maximum response of the secretin plus CCK-OP interaction to be less than with CCK-OP alone. There was no change in the dose required to achieve half-maximal response, D50. These studies indicate that: a) CCK-OP has a greater effect on gallbladder contractility than CCK, b) gastrin I has no effect on gallbladder muscle tone, and c) secretin acts as a noncompetitive antagonist of CCK-OP. These findings suggest that gallbladder motor function may be determined in part by the interaction of secretin and CCK rather than solely in response to CCK.

Altered contractility of circular and longitudinal muscle in TNBS-inflamed guinea pig ileum

1997 ◽  
Vol 272 (5) ◽  
pp. G1258-G1267 ◽  
Author(s):  
J. P. Martinolle ◽  
R. Garcia-Villar ◽  
J. Fioramonti ◽  
L. Bueno
Keyword(s):  
Guinea Pig ◽  
Dose Range ◽  
Circular Muscle ◽  
Maximal Response ◽  
Guinea Pig Ileum ◽  
Trinitrobenzenesulfonic Acid ◽  
Response Curves ◽  
Contractile Responses ◽  
Guinea Pig Model

Intestinal motility disorders are often associated with gut inflammation. We evaluated, in vitro under isometric conditions, changes in contractility of longitudinal and circular muscle layers from guinea pig ileum after 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced ileitis. TNBS treatment did not modify length-active tension relationships for both muscle layers, whereas a significant increase in passive tension was observed in the circular muscle response to stretching. Moreover, in both control and inflamed strips at optimal stretch, concentration-response curves to KCl were similar for both layers. In contrast, contractile responses to receptor agonists were differentially altered in both layers in comparison with controls. Thus, in longitudinal strips from TNBS-treated ileum, there was a twofold increase in maximal response (Emax) induced by carbachol and histamine without modification of 50% effective concentration (EC50) values; responses to 5-hydroxytryptamine (5-HT) were not modified; both alpha 1- and alpha 2-adrenoceptor-mediated responses to epinephrine were abolished. In circular strips, inflammation did not affect the Emax induced by carbachol and histamine but led to increased EC50 values; Emax to 5-HT was reduced without change in EC50 values. Moreover, in the dose range used (0.1 nM to 0.1 mM), a maximal response to carbachol was not obtained in inflamed circular strips. The results indicate that in the guinea pig model of TNBS-induced ileitis, the in vitro contractile responses of circular and longitudinal smooth muscle to the stimulation of various receptors are differentially altered, whereas non-receptor-mediated contraction to KCl depolarization is not modified.

Characterization of leukotriene-induced contraction of the guinea-pig gallbladder in vitro

1993 ◽  
Vol 71 (2) ◽  
pp. 145-150 ◽  
Author(s):  
Stephen M. Freedman ◽  
John L. Wallace ◽  
Eldon A. Shaffer
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Contractile Response ◽  
Disease Process ◽  
Gallstone Formation ◽  
Calcium Stores ◽  
Excitatory Effect ◽  
Gallbladder Contraction ◽  
Biliary Pain

Metabolites of arachidonic acid like prostaglandins have an established role in the pathogenesis of gallstone formation and cholecystitis, but any contribution by leukotrienes is less clear. Leukotrienes might contribute to the disease process by contracting the inflamed and (or) obstructed gallbladder, resulting in further inflammatory damage and biliary pain. To better define the role of leukotrienes, we assessed their effects on gallbladder contracility in vitro. Both leukotriene C4 (LTC4) and D4 (LTD4) had a concentration-dependent excitatory effect on guinea-pig gallbladder smooth muscle. The LTD4-receptor antagonist MK-571 (1 μM) competitively depressed the contractile response, to both LTD4 and LTC4. The source of calcium was defined using ryanodine to deplete intracellular calcium stores and nifedipine to block extracellular entry. Ryanodine (10 μM) antagonized gallbladder contraction at low concentrations of LTD4 (10−10 and 10−9 M). Nifedipine (1 μM) had a greater inhibitory effect on the contractile response at high concentrations of LTD4 (10−8–10−6 M). LTD4-induced contractions were unaffected in tissues pretreated with the neural blocker tetrodotoxin or the muscarinic antagonist atropine. Thus, leukotrienes act directly on the gallbladder smooth muscle, causing contraction at concentrations found in models of cholecystitis, suggesting that these inflammatory mediators contribute to the symptoms and morbidity associated with gallbladder disease.Key words: gallstones, cholecystitis, guinea-pig, gallbladder, leukotriene.

Efffect of vasoactive intestinal polypeptide on gallbladder smooth muscle in vitro.

1978 ◽  
Vol 234 (1) ◽  
pp. E44 ◽  
Author(s):  
J P Ryan ◽  
S Ryave
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Motor Activity ◽  
Vasoactive Intestinal Polypeptide ◽  
Muscle Tone ◽  
Contractile Activity ◽  
Gastrointestinal Hormones ◽  
Resting Tension ◽  
Intestinal Polypeptide

The effect of vasoactive intestinal polypeptide (VIP) on basal and octapeptide of cholecystokinin (OP-CCK) induced tension was examined with guinea pig gallbladder smooth muscle strips in vitro. VIP alone produced dose-related decreases in resting tension and antagonized spontaneous contractile activity where present. In combination with OP-CCK, VIP decreased the expected contractile respone. The degree of antagonism depended upon the concentrations of OP-CCK and VIP. VIP had no effect on acetylcholine-induced contractions. From these observations, we propose that VIP can affect gallbladder motor activity by decreaseing smooth muscle tone and by antagonizing cholecystokinin. These findings lend further support to our proposal that gallbladder motor function may depend upon the action and interaction of the gastrointestinal hormones.

Calcitonin gene-related peptide: am inhibitor of guinea pig gallbladder contraction

1991 ◽  
Vol 69 (8) ◽  
pp. 1149-1154 ◽  
Author(s):  
Loren W. Kline ◽  
Toyoji Kaneko ◽  
Christina G. Benishin ◽  
Peter K. T. Pang
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Colchicine Treatment ◽  
Calcitonin Gene Related Peptide ◽  
Nerve Fibers ◽  
Gallbladder Contraction ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Site Of Action

Calcitonin geae-related peptide (CGRP) relaxes vascular and intestinal smooth muscle. This study localized CGRP in the guinea pig gallbladder, examined the effects of CGRP on KCl- and ACh-induced contraction, and determined CGRPs site of action in the gallbladder. The gallbladder of male Hartley guinea pigs was used in in vitro tension studies, radioimmunoassay, or immunocytochemical studies. Radioimmunoassay showed that 8.0 ± 0.5 pmol/g of immunoreactive CGRP was present. Immunocytochemistry demonstrated that immunoreactive-CGRP nerve fibers occurred around blood vessels, in gallbladder smooth muscle layers, and were associated with ganglia. No immunoreactive cell bodies were observed, even after colchicine treatment. The in vitro tension studies showed that CGRP inhibits either KCl- or acetylcholine-stimulated contraction. CGRP may in part act directly on the gallbladder smooth muscle to inhibit contraction.Key words: calcitonin gene-related peptide, gallbladder, smooth muscle.

Inhibition of dihydropyridine-sensitive calcium entry in hypoxic relaxation of airway smooth muscle

1995 ◽  
Vol 268 (2) ◽  
pp. L201-L206 ◽  
Author(s):  
C. Vannier ◽  
T. L. Croxton ◽  
L. S. Farley ◽  
C. A. Hirshman
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Muscle Tone ◽  
Bay K 8644 ◽  
O2 Concentration ◽  
Voltage Dependent ◽  
Progressive Hypoxia ◽  
Carbamyl Choline

Hypoxia dilates airways in vivo and reduces active tension of airway smooth muscle in vitro. To determine whether hypoxia impairs Ca2+ entry through voltage-dependent channels (VDC), we tested the ability of dihydropyridines to modulate hypoxia-induced relaxation of KCl- and carbamyl choline (carbachol)-contracted porcine bronchi. Carbachol- or KCl-contracted bronchial rings were exposed to progressive hypoxia in the presence or absence of 1 microM BAY K 8644 (an L-type-channel agonist). In separate experiments, rings were contracted with carbachol or KCl, treated with nifedipine (a VDC antagonist), and finally exposed to hypoxia. BAY K 8644 prevented hypoxia-induced relaxation in KCl-contracted bronchi. Nifedipine (10(-5) M) totally relaxed KCl- contracted bronchi. Carbachol-contracted bronchi were only partially relaxed by nifedipine but were completely relaxed when the O2 concentration of the gas was reduced from 95 to 0%. These data indicate that hypoxia can reduce airway smooth muscle tone by limiting entry of Ca2+ through a dihydropyridine-sensitive pathway, but that other mechanisms also contribute to hypoxia-induced relaxation of carbachol-contracted bronchi.

scholarly journals A smooth muscle tone-dependent stretch-activated migrating motor pattern in isolated guinea-pig distal colon

2003 ◽  
Vol 551 (3) ◽  
pp. 955-969 ◽  
Author(s):  
T. K Smith ◽  
G. R Oliver ◽  
G. W Hennig ◽  
D. M O'Shea ◽  
P. V. Berghe ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscle Tone ◽  
Motor Pattern ◽  
Distal Colon ◽  
Smooth Muscle Tone

scholarly journals Tumour necrosis factor-α induces hyperreactivity in tracheal smooth muscle of the guinea-pig in vitro

1998 ◽  
Vol 12 (1) ◽  
pp. 45-49 ◽  
Author(s):  
H-J. Pennings ◽  
K. Kramer ◽  
A. Bast ◽  
W.A. Buurman ◽  
E.F.M. Wouters
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tracheal Smooth Muscle ◽  
Factor I ◽  
Necrosis Factor

Absence of nonadrenergic noncholinergic relaxation in the cat cervical trachea

1988 ◽  
Vol 65 (6) ◽  
pp. 2524-2530 ◽  
Author(s):  
H. Don ◽  
D. G. Baker ◽  
C. A. Richardson
Keyword(s):  
Smooth Muscle ◽  
Vagal Stimulation ◽  
Muscle Tone ◽  
Dynamic Compliance ◽  
Tracheal Mucosa ◽  
In Vivo Experiments ◽  
Lower Airways ◽  
Cervical Trachea

Published in vivo experiments have not supported in vitro reports of the presence of nonadrenergic noncholinergic (NANC) inhibitory pathways in the cat trachea. We therefore examined these pathways, measuring tension in an innervated tracheal segment, flow resistance in more distal airways, and dynamic compliance, in 10 anesthetized mechanically ventilated cats. Initially, cervical vagal stimulation evoked contraction followed by relaxation of smooth muscle of trachea and lower airways; sympathetic stimulation evoked relaxation only. After muscarinic blockade and restoration of smooth muscle tone with 5-hydroxytryptamine (5-HT) applied topically to the tracheal mucosa, vagal stimulation did not affect tracheal segment tension, whereas sympathetic-evoked relaxation was preserved. Similar results were found when tone was restored with intravenous 5-HT, with vagal stimulation also decreasing resistance and increasing compliance. We conclude that NANC pathways are present in lower airways but not in the cervical trachea of the cat. We hypothesize that parasympathetic constriction of cat airway smooth muscle can occur without simultaneous NANC activation, whereas NANC activity occurs only in tandem with parasympathetic stimulation.

Bioactivity of cholecystokinin analogues: CCK-8 is not more potent than CCK-33

1984 ◽  
Vol 247 (1) ◽  
pp. G105-G111 ◽  
Author(s):  
T. E. Solomon ◽  
T. Yamada ◽  
J. Elashoff ◽  
J. Wood ◽  
C. Beglinger
Keyword(s):  
Guinea Pig ◽  
Pancreatic Secretion ◽  
Gallbladder Contraction ◽  
Bathing Medium ◽  
Structural Analogues ◽  
Biological Actions

We determined the relative molar potencies of structural analogues of porcine cholecystokinin (CCK-39, CCK-33, CCK-8, and caerulein). Peptide concentrations delivered in infusates or present in bathing medium were measured by radioimmunoassay. The presence of albumin prevented loss of CCK-39 and CCK-33 from solution to a greater degree than loss of CCK-8 and caerulein from solution. As much as 10-fold differences in CCK-33 and CCK-39 concentrations were seen in albumin-containing versus nonalbumin-containing infusates. The potency estimates calculated from radioimmunoassay-corrected concentrations with CCK-8 as standard (potency 1.00) were canine pancreatic secretion in vivo: CCK-39 4.1, CCK-33 2.2, and caerulein 2.1; rat pancreatic secretion in vivo: CCK-39 2.1, CCK-33 5.4, and caerulein 5.4; rat pancreatic secretion in vitro: CCK-33 1.7, and caerulein 1.2; guinea pig gallbladder contraction in vivo: CCK-33 1.3, and caerulein 0.9; and guinea pig gallbladder contraction in vitro: CCK-33 1.8, and caerulein 5.8. Our data indicate that CCK-8 is not more potent than longer analogues and suggest that larger forms of CCK may be important mediators of the biological actions of CCK.

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