Dexamethasone modifies morphine-, atropine-, verapamil-induced constipation in mice

Calignano, Antonio; Capasso, Anna; Persico, Paola; Mancuso, F.; Sorrentino, L.

doi:10.1016/0306-3623(92)90161-c

Cited by 5 publications

(5 citation statements)

References 17 publications

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“…The urinary disturbance and inhibition of peristalsis become evident at relatively high dosages. Consistent with the intact gut appearance of M 2 Ϫ/ϪM 3 Ϫ/Ϫ mutant mice, it was reported that acute administration of a high dose of atropine did not block gut motility completely (Ruwart et al, 1979;Calignano et al, 1992).…”

Section: In Vivo Significance Of Cholinergic Contractions In Visceralsupporting

confidence: 56%

Mice Lacking M₂and M₃Muscarinic Acetylcholine Receptors Are Devoid of Cholinergic Smooth Muscle Contractions But Still Viable

et al. 2002

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Cholinergic agents elicit prominent smooth muscle contractions via stimulation of muscarinic receptors that comprise five distinct subtypes (M1-M5). Although such contractions are important for autonomic organs, the role of each subtype has not been characterized precisely because of the poor selectivity of the currently available muscarinic ligands. Here, we generated a mutant mouse line (M2-/-M3-/- mice) lacking M2 and M3 receptors that are implicated in such cholinergic contractions. The relative contributions of M2 and M3 receptors in vitro was approximately 5 and 95% for the detrusor muscle contraction and approximately 25 and 75% for the ileal longitudinal muscle contraction, respectively. Thus, M1, M4, or M5 receptors do not seem to play a role in such contractions. Despite the complete lack of cholinergic contractions in vitro, M2-/-M3-/- mice were viable, fertile, and free of apparent intestinal complications. The urinary bladder was distended only in males, which excludes a major contribution by cholinergic mechanisms to the urination in females. Thus, cholinergic mechanisms are dispensable in gastrointestinal motility and female urination. After 10 Hz electrical field stimulation, noncholinergic inputs were found to be increased in the ileum of M2-/-M3-/- females, which may account for the lack of apparent functional deficits. Interestingly, the M2-/-M3-/- mice had smaller ocular pupils than M3-deficient mice. The results suggest a novel role of M2 in the pupillary dilation, contrary to the well known cholinergic constriction. These results collectively suggest that an additional mechanism operates in the control of pupillary constriction-dilatation.

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Section: In Vivo Significance Of Cholinergic Contractions In Visceralsupporting

confidence: 56%

Mice Lacking M₂and M₃Muscarinic Acetylcholine Receptors Are Devoid of Cholinergic Smooth Muscle Contractions But Still Viable

et al. 2002

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“…The finding that verapamil did not suppress the basal gastrointestinal transit (see Figure 4) is in agreement with the work by di carlo et al . (1993) , while some other studies have revealed decreased gastrointestinal transit following verapamil ( Shah et al ., 1987 ; Calignano et al ., 1992 ). The effectiveness of verapamil in the resting state might vary with experimental conditions such as the strain or size of mice employed.…”

Section: Discussionmentioning

confidence: 99%

In vivo evidence that protease‐activated receptors 1 and 2 modulate gastrointestinal transit in the mouse

Kawabata

Kuroda

Nagata

et al. 2001

British J Pharmacology

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1 Protease-activated receptors (PARs) 1 and 2 modulate the gastric and intestinal smooth muscle motility in vitro. In the present study, we examined if activation of PAR-2 and PAR-1 could alter gastrointestinal transit in mice. 2 Intraperitoneal administration of the PAR-2-activating peptide SLIGRL-NH 2 , but not the inactive control LSIGRL-NH 2 , at 1±5 mmol kg 71 , in combination with the aminopeptidase inhibitor amastatin at 2.5 mmol kg 71 , facilitated gastrointestinal transit in a dose-dependent manner. The human PAR-1-derived peptide SFLLR-NH 2 and the speci®c PAR-1 agonist TFLLR-NH 2 , but not the inactive control FSLLR-NH 2 , at 2.5 ± 10 mmol kg 71 , in combination with amastatin, also promoted gastrointestinal transit. 3 The Ca 2+ -activated, small conductance K + channel inhibitor apamin at 0.01 mmol kg 71 signi®cantly potentiated the actions of SLIGRL-NH 2 and TFLLR-NH 2 at sube ective doses. 4 The increased gastrointestinal transit exerted by either SLIGRL-NH 2 at 5 mmol kg 71 or TFLLR-NH 2 at 10 mmol kg 71 was completely abolished by the L-type Ca 2+ channel inhibitor verapamil at 61.6 mmol kg 71 . In contrast, the tyrosine kinase inhibitor genistein at 18.5 mmol kg 71 failed to modify the e ects of the agonists for PAR-2 or PAR-1. 5 These ®ndings demonstrate that PAR-1 and PAR-2 modulate gastrointestinal transit in mice in vivo. Our data also suggest that the PAR-1-and PAR-2-mediated e ects are modulated by apaminsensitive K + channels and are dependent on activation of L-type Ca 2+ channels, but independent of tyrosine kinase. Our study thus provides novel evidence for the physiological and/or pathophysiological roles of PARs 1 and 2 in the digestive systems, most probably during in¯ammation.

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“…The aim of this study was therefore: a) to confirm whether a fasting period of six hours was an optimal fast for assessing intestinal transit, as well as gastric emptying; and b) to establish the welfare benefits of a reduction in the fasting period by assessing body weight and housing conditions for mice. Atropine is known to reduce gastric emptying and intestinal transit in both rodents (8,12,18,24) and humans (25,26), and was included in this study as a standard reference compound.…”

Section: Introductionmentioning

confidence: 99%

Refinement of the Charcoal Meal Study by Reduction of the Fasting Period

et al. 2012

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The aim of this investigation was to determine whether a shorter fasting period than the one historically employed for the charcoal meal test, could be used when measuring gastric emptying and intestinal transit within the same animal, and to ascertain whether the scientific outcome would be affected by this benefit to animal welfare. Rats and mice were fasted for 0, 3, 6 or 18 hours before the oral administration of vehicle or atropine. One hour later, the animals were orally administered a charcoal meal, then 20 minutes later, they were killed and the stomach and small intestine were removed. Intestinal transit time (the position of the charcoal front as a percentage of the total length of the small intestine) and relative gastric emptying (weight of stomach contents) were measured. Rats and mice fasted for six hours showed results for gastric emptying and intestinal transit which were similar to those obtained in animals fasted for 18 hours. Reducing the fasting period reduced the body weight loss in both species, and mice on shorter fasts could be group-housed, as hunger-induced fighting was lessened. Therefore, a fasting period of six hours was subsequently adopted for charcoal meal studies at our institution.

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Dexamethasone modifies morphine-, atropine-, verapamil-induced constipation in mice

Cited by 5 publications

References 17 publications

Mice Lacking M₂and M₃Muscarinic Acetylcholine Receptors Are Devoid of Cholinergic Smooth Muscle Contractions But Still Viable

Mice Lacking M₂and M₃Muscarinic Acetylcholine Receptors Are Devoid of Cholinergic Smooth Muscle Contractions But Still Viable

In vivo evidence that protease‐activated receptors 1 and 2 modulate gastrointestinal transit in the mouse

Refinement of the Charcoal Meal Study by Reduction of the Fasting Period

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Dexamethasone modifies morphine-, atropine-, verapamil-induced constipation in mice

Cited by 5 publications

References 17 publications

Mice Lacking M2and M3Muscarinic Acetylcholine Receptors Are Devoid of Cholinergic Smooth Muscle Contractions But Still Viable

Mice Lacking M2and M3Muscarinic Acetylcholine Receptors Are Devoid of Cholinergic Smooth Muscle Contractions But Still Viable

In vivo evidence that protease‐activated receptors 1 and 2 modulate gastrointestinal transit in the mouse

Refinement of the Charcoal Meal Study by Reduction of the Fasting Period

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Mice Lacking M₂and M₃Muscarinic Acetylcholine Receptors Are Devoid of Cholinergic Smooth Muscle Contractions But Still Viable

Mice Lacking M₂and M₃Muscarinic Acetylcholine Receptors Are Devoid of Cholinergic Smooth Muscle Contractions But Still Viable