D-1 Dopamine Receptors Mediate Dopamine-Induced Pancreatic Exocrine Secretion in Anesthetized Dogs
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- Iwatsuki Kazuhiko
- the Department of Pharmacology, Shinshu University School of Medicine
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- Horiuchi Akira
- the Department of Pharmacology, Shinshu University School of Medicine
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- Ren Lei-Ming
- the Department of Pharmacology, Shinshu University School of Medicine
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- Chiba Shigetoshi
- the Department of Pharmacology, Shinshu University School of Medicine
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Abstract
Characterization of dopamine (DA) receptor subtypes was examined on the canine exocrine pancreas using selective DA receptor agonists and antagonists in anesthetized dogs. Each drug was injected i.a. in a single bolus fashion. Graded doses of DA (0.01-3μmol) produced dose-dependent increases in the secretory rate of pancreatic juice, with a maximum effect at approximately 1μmol. SCH23390 (3-30nmol), a selective D-1 DA receptor antagonist, caused a progressive parallel shift to the right in the dose-response curve for DA-induced pancreatic secretion without changes in the maximal response. However, domperidone (3μmol), a selective D-2 DA receptor antagonist, did not antagonize the DA-induced pancreatic exocrine secretion. A Schild analysis of the data indicates that the inhibitory constant value for SCH23390 to inhibit DA-stimulated secretion was 6.9nmol. In addition, the stimulatory effects of SKF38393 (0.1-10μmol) and YM435 (0.3-30nmol), selective D-1 DA receptor agonists, and LY171555 (1-10μmol), a selective D-2 DA receptor agonist, on pancreatic secretion were demonstrated. The rank order of agonist potency was YM435>DA>SKF38393_??_LY171555. These results suggest that DA-induced pancreatic exocrine secretion is mediated by activation of D-1 DA receptors. (Hypertens Res 1995; 18 Suppl. I: S173-S174)
Journal
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- Hypertension Research
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Hypertension Research 18 (SupplementI), S173-S174, 1995
The Japanese Society of Hypertension
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Details 詳細情報について
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- CRID
- 1390001204719550720
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- NII Article ID
- 10008736022
- 130003399336
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- NII Book ID
- AA10847079
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- ISSN
- 13484214
- 09169636
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- Text Lang
- en
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- Data Source
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- JaLC
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed