ウサギ耳動脈におけるプリン作動性ノルエピネフリン遊離促進機構に関する研究
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- Material Type
- 記事
- Author/Editor
- 野澤(石井) 玲子篠塚 和正国友 勝 他
- Periodical title
- 薬学雑誌 = Journal of the Pharmaceutical Society of Japan / 日本薬学会 編
- No. or year of volume/issue
- 119(6) 1999.06
- Volume
- 119
- Issue
- 6
- Pages
- 417～428
- Publication date of volume/issue (W3CDTF)
- 1999-06
- ISSN (Periodical Title)
- 0031-6903
- ISSN-L (Periodical Title)
- 0031-6903
- Publication (Periodical Title)
- 東京 : 日本薬学会
- Place of Publication (Country Code)
- JP
- Text Language Code
- jpn
- NDLC
- Target Audience
- 一般
- Holding library
- 国立国会図書館
- Call No.
- Z19-411
- Data Provider (Database)
- 国立国会図書館 : 国立国会図書館雑誌記事索引
- Bibliographic ID (NDL)
- 4741023
- Bibliographic Record Category (NDL)
- 632
- Summary, etc.
- The purinergic modulation of the release of norepinephrine (NE) from sympathetic nerves in the rabbit ear artery was investigated. Methoxamine, an α<SUB>1</SUB>-adrenoceptor agonist, enhanced the NE-release by electrical stimulation (ES) and released large amounts of adenyl purines (ATP, ADP, AMP and adenosine) from the endothelium. Both actions of methoxamine were blocked by prazosin. In addition, the enhancement of the NE-release by methoxamine was abolished by 8-sulfophenyl theophylline (8SPT), a P1-purinoceptor antagonist. These findings indicated that the endogenous purines and purinoceptors participate in the facilitation of NE-release by α<SUB>1</SUB>-adrenoceptor stimulation. P1-Purinoceptor agonists, such as adenosine and 2-chloroadenosine, and P2-purinoceptor agonists, such as ATP and β, γ-methylene ATP (βγ-mATP), enhanced the ES-evoked NE-release. This enhancement was antagonized not only by the P1-purinoceptor antagonist, 8SPT, but also by the P2-purinoceptor desensitizing agent, α, β-methylene ATP. A phosphodiesterase inhibitor, Ro20-1724 potentiates the enhancement of NE-release by βγ-mATP. On the other hand, an adenylate cyclase inhibitor, SQ22536, inhibited the enhancement of NE-release by βγ-mATP. These findings suggested that prejunctional facilitatory purinoceptors exist on the adrenergic nerves of the rabbit ear artery. This receptor may be coupled to adenylate cyclase and is different from well-known P1 and P2 purinoceptors. In the rabbit ear artery, adrenergic neurotransmission may be regulated by endogenous ATP and its metabolites via prejunctional facilitatory purinoceptors, which were initiated by α<SUB>1</SUB>-adrenoceptor stimulation; i.e. transsynaptic regulation of neurotransmission.
- DOI
- 10.1248/yakushi1947.119.6_417
- Access Restrictions
- インターネット公開
- Data Provider (Database)
- 科学技術振興機構 : J-STAGE
- Summary, etc.
- The purinergic modulation of the release of norepinephrine (NE) from sympathetic nerves in the rabbit ear artery was investigated. Methoxamine, an α<SUB>1</SUB>-adrenoceptor agonist, enhanced the NE-release by electrical stimulation (ES) and released large amounts of adenyl purines (ATP, ADP, AMP and adenosine) from the endothelium. Both actions of methoxamine were blocked by prazosin. In addition, the enhancement of the NE-release by methoxamine was abolished by 8-sulfophenyl theophylline (8SPT), a P1-purinoceptor antagonist. These findings indicated that the endogenous purines and purinoceptors participate in the facilitation of NE-release by α<SUB>1</SUB>-adrenoceptor stimulation. P1-Purinoceptor agonists, such as adenosine and 2-chloroadenosine, and P2-purinoceptor agonists, such as ATP and β, γ-methylene ATP (βγ-mATP), enhanced the ES-evoked NE-release. This enhancement was antagonized not only by the P1-purinoceptor antagonist, 8SPT, but also by the P2-purinoceptor desensitizing agent, α, β-methylene ATP. A phosphodiesterase inhibitor, Ro20-1724 potentiates the enhancement of NE-release by βγ-mATP. On the other hand, an adenylate cyclase inhibitor, SQ22536, inhibited the enhancement of NE-release by βγ-mATP. These findings suggested that prejunctional facilitatory purinoceptors exist on the adrenergic nerves of the rabbit ear artery. This receptor may be coupled to adenylate cyclase and is different from well-known P1 and P2 purinoceptors. In the rabbit ear artery, adrenergic neurotransmission may be regulated by endogenous ATP and its metabolites via prejunctional facilitatory purinoceptors, which were initiated by α<SUB>1</SUB>-adrenoceptor stimulation; i.e. transsynaptic regulation of neurotransmission.
- DOI
- 10.1248/yakushi1947.119.6_41710.1002/chin.199940267
- Access Restrictions
- インターネット公開
- Related Material (URI)
- Data Provider (Database)
- 国立情報学研究所 : CiNii Research
- Original Data Provider (Database)
- Japan Link Center雑誌記事索引データベースCrossrefCiNii Articles
- Bibliographic ID (NDL)
- 4741023
- NAID
- 110003648749