Effects of Adrenoceptor Antagonists on the Cutaneous Blood Flow Increase Response to Sympathetic Nerve Stimulation in Rats with Persistent Inflammation.
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- Koeda Tomoko
- Department of Neural Regulation, Research Institute of Environmental Medicine, Nagoya University
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説明
There is some evidence that the sympathetic nervous system plays a role in the development and/or maintenance of painful states, and that sympathetic nervous function is altered in these conditions. Our previous experiments showed that electrical stimulation of the lumbar sympathetic trunk (sympathetic stimulation: SS), which normally induces a decrease in blood flow (BF) of plantar skin, induced its BF increase in about 50% of adjuvant-inflamed rats. To investigate the mechanism of this BF-increase response, we examined whether noradrenaline (NA) plays any role in this changed response to SS, and which receptor subtype is involved. We measured paw cutaneous BF response with a laser Doppler flowmeter in rats chronically inflamed with complete Freund's adjuvant. SS induced the BF-increase response in 50–67% of measured sites. Close-arterially injected NA induced the BF-increase response at dosages between 10–100 ng/kg only at the sites with the BF-increase response to SS. The BF-increase and -decrease responses to NA was significantly reduced after the close-arterial injection of either α1- or α2-adrenoceptor antagonists (p lt; 0.05, respectively). In contrast, although the BF-decrease responses to SS were significantly reduced by administration of α1- and α2-adrenoceptor antagonist, BF-increase response was reduced only by α1-adrenoceptor antagonist, and that only at a higher dose. In addition, the β-adrenoceptor antagonist had no effects on both responses. These results suggest that the BF-increase response to SS involves, additionally to NA, a non-adrenergic mechanism.<br>
収録刊行物
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- The Japanese Journal of Physiology
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The Japanese Journal of Physiology 52 (6), 521-530, 2002
一般社団法人 日本生理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205042924288
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- NII論文ID
- 130004435851
- 30015529794
- 50000764305
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- NII書誌ID
- AA00691224
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- COI
- 1:CAS:528:DC%2BD3sXis1Oku7c%3D
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- ISSN
- 18811396
- 0021521X
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- NDL書誌ID
- 6465745
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- PubMed
- 12617758
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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