Effects of cisapride on feline colonic smooth muscle function

Robert J. Washabau, Jill Sammarco

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Objective - To determine the effects of cisapride on feline colonic smooth muscle function. Design - In vitro smooth muscle mechanical measurements. Animals - Intact colon was obtained from healthy 2- or 3-year-old cats. Procedure - Longitudinal smooth muscle strips from proximal and distal portions of feline colon were suspended in physiologic buffer solution (37 °C, 100% O2, pH 7.4), attached to isometric force transducers, and stretched to optimal muscle length. Control responses were obtained at each muscle site with acetylcholine (10-8 to 10-4 M), cholecystokinin (10-11 to 10-7 M), substance P (10-11 to 10-7 M), or neurotensin (10-11 to 10-7 M). Muscles were then stimulated with cumulative (10-9 to 10-6 M) or bolus (10-6 M) doses of cisapride in the absence or presence of tetrodotoxin (10-6 M) and atropine (10-6 M), nifedipine (10-6 M), or calcium-free buffer solution. Results - Cisapride stimulated contractions of longitudinal smooth muscle from proximal and distal portions of feline colon that were similar in magnitude to contractions induced by substance P and neurotensin. Cisapride contractions were only partially inhibited by tetrodotoxin (10-6 M) and atropine (10-6 M), suggesting that cisapride responses are only partially dependent on enteric cholinergic nerves. Nifedipine (10-6 M) inhibited the maximal contraction to cisapride (10-6 M) by approximately 80%. Removal of extracellular calcium did not inhibit cisapride contractions to a greater extent than did inhibition by nifedipine, indicating that calcium influx through voltage-dependent calcium channels was predominantly responsible for the dependence of the cisapride contraction on extracellular calcium. Conclusions - Cisapride-induced contractions of feline colonic smooth muscle are largely smooth muscle-mediated and dependent on calcium influx, and are only partially dependent on enteric cholinergic nerves. Clinical Relevance - Cisapride may be useful in the treatment of feline colonic motility disorders.

Original languageEnglish (US)
Pages (from-to)541-546
Number of pages6
JournalAmerican journal of veterinary research
Volume57
Issue number4
StatePublished - Apr 1 1996

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Cisapride
Felidae
smooth muscle
Smooth Muscle
cats
calcium
colon
tetrodotoxin
substance P
cholinergic agents
atropine
Calcium
Nifedipine
muscles
nerve tissue
buffers
Neurotensin
Colon
Tetrodotoxin
Substance P

Cite this

Effects of cisapride on feline colonic smooth muscle function. / Washabau, Robert J.; Sammarco, Jill.

In: American journal of veterinary research, Vol. 57, No. 4, 01.04.1996, p. 541-546.

Research output: Contribution to journalArticle

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title = "Effects of cisapride on feline colonic smooth muscle function",
abstract = "Objective - To determine the effects of cisapride on feline colonic smooth muscle function. Design - In vitro smooth muscle mechanical measurements. Animals - Intact colon was obtained from healthy 2- or 3-year-old cats. Procedure - Longitudinal smooth muscle strips from proximal and distal portions of feline colon were suspended in physiologic buffer solution (37 °C, 100{\%} O2, pH 7.4), attached to isometric force transducers, and stretched to optimal muscle length. Control responses were obtained at each muscle site with acetylcholine (10-8 to 10-4 M), cholecystokinin (10-11 to 10-7 M), substance P (10-11 to 10-7 M), or neurotensin (10-11 to 10-7 M). Muscles were then stimulated with cumulative (10-9 to 10-6 M) or bolus (10-6 M) doses of cisapride in the absence or presence of tetrodotoxin (10-6 M) and atropine (10-6 M), nifedipine (10-6 M), or calcium-free buffer solution. Results - Cisapride stimulated contractions of longitudinal smooth muscle from proximal and distal portions of feline colon that were similar in magnitude to contractions induced by substance P and neurotensin. Cisapride contractions were only partially inhibited by tetrodotoxin (10-6 M) and atropine (10-6 M), suggesting that cisapride responses are only partially dependent on enteric cholinergic nerves. Nifedipine (10-6 M) inhibited the maximal contraction to cisapride (10-6 M) by approximately 80{\%}. Removal of extracellular calcium did not inhibit cisapride contractions to a greater extent than did inhibition by nifedipine, indicating that calcium influx through voltage-dependent calcium channels was predominantly responsible for the dependence of the cisapride contraction on extracellular calcium. Conclusions - Cisapride-induced contractions of feline colonic smooth muscle are largely smooth muscle-mediated and dependent on calcium influx, and are only partially dependent on enteric cholinergic nerves. Clinical Relevance - Cisapride may be useful in the treatment of feline colonic motility disorders.",
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N2 - Objective - To determine the effects of cisapride on feline colonic smooth muscle function. Design - In vitro smooth muscle mechanical measurements. Animals - Intact colon was obtained from healthy 2- or 3-year-old cats. Procedure - Longitudinal smooth muscle strips from proximal and distal portions of feline colon were suspended in physiologic buffer solution (37 °C, 100% O2, pH 7.4), attached to isometric force transducers, and stretched to optimal muscle length. Control responses were obtained at each muscle site with acetylcholine (10-8 to 10-4 M), cholecystokinin (10-11 to 10-7 M), substance P (10-11 to 10-7 M), or neurotensin (10-11 to 10-7 M). Muscles were then stimulated with cumulative (10-9 to 10-6 M) or bolus (10-6 M) doses of cisapride in the absence or presence of tetrodotoxin (10-6 M) and atropine (10-6 M), nifedipine (10-6 M), or calcium-free buffer solution. Results - Cisapride stimulated contractions of longitudinal smooth muscle from proximal and distal portions of feline colon that were similar in magnitude to contractions induced by substance P and neurotensin. Cisapride contractions were only partially inhibited by tetrodotoxin (10-6 M) and atropine (10-6 M), suggesting that cisapride responses are only partially dependent on enteric cholinergic nerves. Nifedipine (10-6 M) inhibited the maximal contraction to cisapride (10-6 M) by approximately 80%. Removal of extracellular calcium did not inhibit cisapride contractions to a greater extent than did inhibition by nifedipine, indicating that calcium influx through voltage-dependent calcium channels was predominantly responsible for the dependence of the cisapride contraction on extracellular calcium. Conclusions - Cisapride-induced contractions of feline colonic smooth muscle are largely smooth muscle-mediated and dependent on calcium influx, and are only partially dependent on enteric cholinergic nerves. Clinical Relevance - Cisapride may be useful in the treatment of feline colonic motility disorders.

AB - Objective - To determine the effects of cisapride on feline colonic smooth muscle function. Design - In vitro smooth muscle mechanical measurements. Animals - Intact colon was obtained from healthy 2- or 3-year-old cats. Procedure - Longitudinal smooth muscle strips from proximal and distal portions of feline colon were suspended in physiologic buffer solution (37 °C, 100% O2, pH 7.4), attached to isometric force transducers, and stretched to optimal muscle length. Control responses were obtained at each muscle site with acetylcholine (10-8 to 10-4 M), cholecystokinin (10-11 to 10-7 M), substance P (10-11 to 10-7 M), or neurotensin (10-11 to 10-7 M). Muscles were then stimulated with cumulative (10-9 to 10-6 M) or bolus (10-6 M) doses of cisapride in the absence or presence of tetrodotoxin (10-6 M) and atropine (10-6 M), nifedipine (10-6 M), or calcium-free buffer solution. Results - Cisapride stimulated contractions of longitudinal smooth muscle from proximal and distal portions of feline colon that were similar in magnitude to contractions induced by substance P and neurotensin. Cisapride contractions were only partially inhibited by tetrodotoxin (10-6 M) and atropine (10-6 M), suggesting that cisapride responses are only partially dependent on enteric cholinergic nerves. Nifedipine (10-6 M) inhibited the maximal contraction to cisapride (10-6 M) by approximately 80%. Removal of extracellular calcium did not inhibit cisapride contractions to a greater extent than did inhibition by nifedipine, indicating that calcium influx through voltage-dependent calcium channels was predominantly responsible for the dependence of the cisapride contraction on extracellular calcium. Conclusions - Cisapride-induced contractions of feline colonic smooth muscle are largely smooth muscle-mediated and dependent on calcium influx, and are only partially dependent on enteric cholinergic nerves. Clinical Relevance - Cisapride may be useful in the treatment of feline colonic motility disorders.

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