Special Sensitization Pattern in Adenosine-Induced Myocardial Responses After Thyroxine-Treatment
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- Gesztelyi Rudolf
- Department of Pharmacology and Pharmacotherapy, University of Debrecen, Medical-and Health Science Center
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- Zsuga Judit
- Department of Pharmacology and Pharmacotherapy, University of Debrecen, Medical-and Health Science Center
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- Cseppentõ Ágnes
- Department of Pharmacology and Pharmacotherapy, University of Debrecen, Medical-and Health Science Center
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- Bajza Ágnes
- Department of Pharmacology and Pharmacotherapy, University of Debrecen, Medical-and Health Science Center
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- Varga Angelika
- Department of Pharmacology and Pharmacotherapy, University of Debrecen, Medical-and Health Science Center
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- Szabó Judit Zs.
- Department of Pharmacology and Pharmacotherapy, University of Debrecen, Medical-and Health Science Center
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- Szentmiklósi A. József
- Department of Pharmacology and Pharmacotherapy, University of Debrecen, Medical-and Health Science Center
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Chronic thyroxine treatment reduces the susceptibility of atrial myocardium to adenosine. While the possible role of membrane adenosine receptors in this action is supported by several studies, the involvement of intracellular adenosine mechanisms has not been defined. The present experiments were carried out in electrically driven euthyroid and hyperthyroid guinea pig atrial myocardium. The extracellular and intracellular actions of adenosine were analyzed pharmacologically by the use of specific blockers of membrane adenosine transport and intracellular adenosine deaminase (ADA). The involvement of phosphoprotein phosphatase, phospholamban, and sarcoplasmic reticulum Ca2+ ATPase (SERCA) in the adenosine-induced responses was also studied. The major findings were as follows: i) pD2- and Emax-values for adenosine-induced decrease of mechanical activity were significantly reduced after an 8-day thyroxine treatment in atrial tissues; ii) in atria of thyroxine-treated animals, membrane purine transport inhibitors (dipyridamole, NBTI) induced similar leftward shifts in concentration-response curves for adenosine in both euthyroid and hyperthyroid atrial myocardium without altering the depressed Emax values; iii) the leftward displacement evoked by inhibitors of intracellularly located ADA (coformycin, EHNA) was more striking in hyperthyroid than euthyroid myocardia. ADA inhibitors induced a complete reversal of the maximum adenosine actions; iv) inhibition by cantharidin of phosphoprotein phosphatases (after inhibition of ADA) reduced the adenosine-induced responses. This inhibition was stronger in hyperthyroid atria; v) pharmacological elimination of sarcoplasmic reticulum Ca2+ ATPase by cyclopiazonic acid did not alter the cardiac responses to adenosine and this was independent of thyroid status. It is suggested that distinct modulation of the extra- and intracellular adenosine actions is present in eu- and hyperthyroid hearts. In the latter, a predominance of intracellular adenosine mechanisms can be proposed.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 91 (4), 295-304, 2003
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205177655040
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- NII論文ID
- 130000073688
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 6510776
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- PubMed
- 12719658
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可