Mechanism of Membrane Depolarization Involved in α<sub>1A</sub>-Adrenoceptor-Mediated Contraction in Rat Tail and Iliac Arteries
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- Ishida Hirotake
- Department of Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka
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- Saito Shin-ya
- Department of Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka
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- Dohi Naoki
- Department of Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka
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- Ishikawa Tomohisa
- Department of Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka
Bibliographic Information
- Other Title
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- Mechanism of Membrane Depolarization Involved in α[1A]-Adrenoceptor-Mediated Contraction in Rat Tail and Iliac Arteries
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Abstract
<p>Our previous studies have shown that phenylephrine-induced contraction of cutaneous arteries is primarily mediated via α1A-adrenoceptors, but not α1D-adrenoceptors that generally mediate vascular contraction, and that the larger part of the contraction is induced in a voltage-dependent Ca2+ channel (VDCC)-independent manner. Here, we investigated the mechanism underlying the smaller part of the α1A-adrenoceptor-mediated contraction, i.e., VDCC-dependent one, in cutaneous arteries. Isometric contraction was measured with wire myograph in endothelium-denuded tail and iliac arterial rings isolated from male Wistar rats. LOE908 (10 µM), a cation channel blocker, partially inhibited the contraction induced by phenylephrine in tail and iliac arteries. Nifedipine (10 µM) further suppressed the phenylephrine-induced contraction that remained in the presence of LOE908 (10 µM) in iliac arteries but barely in tail arteries, suggesting that phenylephrine-induced depolarization in tail arteries is due to the activation of LOE908-sensitive cation channels. In iliac arteries, the contraction induced by A-61603, a specific α1A-adrenoceptor agonist, was also partially inhibited by LOE908 (10 µM); however, nifedipine had little effect on the A-61603-induced contraction that remained in the presence of LOE908 (10 µM), suggesting that depolarization mediated via α1A-adrenoceptors is due to the activation of LOE908-sensitive cation channels even in iliac arteries. These results suggest that membrane depolarization mediated via α1Α-adrenoceptors is caused by cation influx through LOE908-sensitive cation channels. Less contribution of VDCC to phenylephrine-induced contraction in tail arteries compared to in iliac arteries is likely due to that α1Α-adrenoceptor-mediated activation of VDCC is caused only by depolarization via cation influx through LOE908-sensitive cation channels.</p>
Journal
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- Biological and Pharmaceutical Bulletin
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Biological and Pharmaceutical Bulletin 42 (10), 1741-1745, 2019-10-01
The Pharmaceutical Society of Japan
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Details 詳細情報について
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- CRID
- 1390564227317600000
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- NII Article ID
- 130007722436
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- NII Book ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL BIB ID
- 029984675
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- PubMed
- 31582662
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- Abstract License Flag
- Disallowed