Abstract
Heart rate responses to i.v. administration of cholecystokinin-8 (CCK-8) were investigated in Otsuka Long-Evans Tokushima Fatty (OLETF) rats lacking CCK-A receptors and control Long-Evans Tokushima Otsuka (LETO) rats. The heart rate decreased after i.v. administration of 3 nmol.kg(-)(1) of CCK-8 in LETO rats, but not in OLETF rats. Bradycardia in the LETO rats disappeared after treatment with MK-329, but not after treatment with L-365,260. The expression of CCK-A receptor precursor mRNA was found exclusively in the atrium in LETO rats. These results suggest that CCK-8 decreases heart rate via CCK-A receptors located in the atrium of the rats.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Benzodiazepinones / pharmacology
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Blotting, Southern
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Bradycardia
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DNA, Complementary / metabolism
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Devazepide / pharmacology
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Dose-Response Relationship, Drug
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Heart Atria / metabolism
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Heart Rate / drug effects*
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Hormone Antagonists / pharmacology
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Male
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Phenylurea Compounds / pharmacology
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Polymerase Chain Reaction
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RNA, Messenger / metabolism
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Rats
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Rats, Inbred OLETF*
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Rats, Long-Evans*
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Receptor, Cholecystokinin A
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Receptors, Cholecystokinin / biosynthesis
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Receptors, Cholecystokinin / genetics*
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Receptors, Cholecystokinin / physiology*
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Sincalide / metabolism
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Sincalide / pharmacology*
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Time Factors
Substances
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Benzodiazepinones
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DNA, Complementary
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Hormone Antagonists
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Phenylurea Compounds
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RNA, Messenger
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Receptor, Cholecystokinin A
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Receptors, Cholecystokinin
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L 365260
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Devazepide
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Sincalide