Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice
Lázaro-Suárez, M. L. ; Gómez-Zamudio, J. H. ; Gallardo-Ortíz, I. A. ; Tanoue, A. ; Tsujimoto, G. ; Farias-Rodríguez, V. M. ; Villalobos-Molina, R.
Oxford, UK : Blackwell Science Ltd
Published 2005
Oxford, UK : Blackwell Science Ltd
Published 2005
| ISSN: |
1474-8673
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| Source: |
Blackwell Publishing Journal Backfiles 1879-2005
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| Topics: |
Chemistry and Pharmacology
Medicine
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| Notes: |
1 We have characterized the α1-adrenoceptor subtypes present in isolated aorta of the α1D-adrenoceptor knockout (KO) mice, by chloroethylclonidine (CEC)-induced alkylation and their protection by selective α1-adrenoceptor antagonists. 2 The α1D-adrenoceptor is involved in the contractile response to noradrenaline in wild type (WT) mouse aorta. 3 In WT mice 5-methylurapidil (5-MU, an α1A-adrenoceptor antagonist) or BMY 7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl] ethyl]-8-azaspiro[4.5] decane-7,9 dione, a selective α1D-adrenoceptor antagonist), protected the receptors from CEC-induced (α1B/D-adrenoceptor) alkylation, the combination of both antagonists resulted in complete protection, while AH11110A (1-[biphenyl-2-yloxy]-4-imino-4-piperidin-1-yl-butan-2-ol, an α1B-adrenoceptor antagonist) did not protect. 4 In aorta of KO mice there was a 19-fold rightward shift in noradrenaline effective concentration (EC50) compared with WT; while 5-MU alone or in combination with AH11110A protected α1-adrenoceptors to the same extent. 5 The data indicate that α1A-adrenoceptors mediate contraction and suggest their role in maintaining homeostasis in the α1D-adrenoceptors KO mice.
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| Type of Medium: |
Electronic Resource
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| URL: |