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: |
| _version_ | 1798290011227947010 |
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| autor | Lázaro-Suárez, M. L. Gómez-Zamudio, J. H. Gallardo-Ortíz, I. A. Tanoue, A. Tsujimoto, G. Farias-Rodríguez, V. M. Villalobos-Molina, R. |
| autorsonst | Tanoue, A. Tsujimoto, G. Farias-Rodríguez, V. M. Villalobos-Molina, R. |
| book_url | http://dx.doi.org/10.1111/j.1474-8673.2005.00348.x |
| datenlieferant | nat_lic_papers |
| hauptsatz | hsatz_simple |
| identnr | NLZ242367895 |
| insertion_date | 2012-04-27 |
| issn | 1474-8673 |
| journal_name | Autonomic & autacoid pharmacology |
| materialart | 1 |
| 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. |
| package_name | Blackwell Publishing |
| publikationsjahr_anzeige | 2005 |
| publikationsjahr_facette | 2005 |
| publikationsjahr_intervall | 7994:2005-2009 |
| publikationsjahr_sort | 2005 |
| publikationsort | Oxford, UK |
| publisher | Blackwell Science Ltd |
| reference | 25 (2005), S. 0 |
| search_space | articles |
| shingle_author_1 | Lázaro-Suárez, M. L. Gómez-Zamudio, J. H. Gallardo-Ortíz, I. A. Tanoue, A. Tsujimoto, G. Farias-Rodríguez, V. M. Villalobos-Molina, R. |
| shingle_author_2 | Lázaro-Suárez, M. L. Gómez-Zamudio, J. H. Gallardo-Ortíz, I. A. Tanoue, A. Tsujimoto, G. Farias-Rodríguez, V. M. Villalobos-Molina, R. |
| shingle_author_3 | Lázaro-Suárez, M. L. Gómez-Zamudio, J. H. Gallardo-Ortíz, I. A. Tanoue, A. Tsujimoto, G. Farias-Rodríguez, V. M. Villalobos-Molina, R. |
| shingle_author_4 | Lázaro-Suárez, M. L. Gómez-Zamudio, J. H. Gallardo-Ortíz, I. A. Tanoue, A. Tsujimoto, G. Farias-Rodríguez, V. M. Villalobos-Molina, R. |
| shingle_catch_all_1 | Lázaro-Suárez, M. L. Gómez-Zamudio, J. H. Gallardo-Ortíz, I. A. Tanoue, A. Tsujimoto, G. Farias-Rodríguez, V. M. Villalobos-Molina, R. Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice Blackwell Science Ltd 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. 1474-8673 14748673 |
| shingle_catch_all_2 | Lázaro-Suárez, M. L. Gómez-Zamudio, J. H. Gallardo-Ortíz, I. A. Tanoue, A. Tsujimoto, G. Farias-Rodríguez, V. M. Villalobos-Molina, R. Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice Blackwell Science Ltd 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. 1474-8673 14748673 |
| shingle_catch_all_3 | Lázaro-Suárez, M. L. Gómez-Zamudio, J. H. Gallardo-Ortíz, I. A. Tanoue, A. Tsujimoto, G. Farias-Rodríguez, V. M. Villalobos-Molina, R. Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice Blackwell Science Ltd 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. 1474-8673 14748673 |
| shingle_catch_all_4 | Lázaro-Suárez, M. L. Gómez-Zamudio, J. H. Gallardo-Ortíz, I. A. Tanoue, A. Tsujimoto, G. Farias-Rodríguez, V. M. Villalobos-Molina, R. Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice Blackwell Science Ltd 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. 1474-8673 14748673 |
| shingle_title_1 | Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice |
| shingle_title_2 | Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice |
| shingle_title_3 | Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice |
| shingle_title_4 | Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice |
| sigel_instance_filter | dkfz geomar wilbert ipn albert |
| source_archive | Blackwell Publishing Journal Backfiles 1879-2005 |
| timestamp | 2024-05-06T08:09:56.664Z |
| titel | Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice |
| titel_suche | Chloroethylclonidine reveals that α1A-adrenoceptors mediate contraction in aorta of α1D-adrenoceptor knockout mice |
| topic | V WW-YZ |
| uid | nat_lic_papers_NLZ242367895 |