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Am J Physiol Heart Circ Physiol 289: H1923-H1932, 2005. First published June 10, 2005; doi:10.1152/ajpheart.00288.2005
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Correlation between mRNA levels and functional role of {alpha}1-adrenoceptor subtypes in arteries: evidence of {alpha}1L as a functional isoform of the {alpha}1A-adrenoceptor

Daniel Martí,2,3,* Raquel Miquel,1,* Khalid Ziani,1 Regina Gisbert,1 M. Dolores Ivorra,1 Elsa Anselmi,1 Lucrecia Moreno,3 Victoria Villagrasa,3 Domingo Barettino,2 and Pilar D'Ocon1,4

1Departamento de Farmacología, Facultad de Farmacia, Universitat de València; 2Instituto de Biomedicina de Valencia, Consejo Superior de Investigaciones Científicas, Valencia; 3Facultad de Ciencias Experimentales y de la Salud, Universidad Cardenal Herrera, Valencia; and 4Unidad Mixta, Centro Nacional de Investigaciones Cardiovasculares—Universitat de València Estudi General, Valencia, Spain

Submitted 23 March 2005 ; accepted in final form 26 May 2005

The mRNA levels for the three {alpha}1-adrenoceptor subtypes, {alpha}1A, {alpha}1B, and {alpha}1D, were quantified by real-time RT-PCR in arteries from Wistar rats. The {alpha}1D-adrenoceptor was prominent in both aorta (79.0%) and mesenteric artery (68.7%), {alpha}1A predominated in tail (61.7%) and small mesenteric artery (73.3%), and both {alpha}1A- and {alpha}1D-subtypes were expressed at similar levels in iliac artery. The mRNA levels of the {alpha}1B-subtype were a minority in all vessels (1.7–11.1%). Concentration-response curves of contraction in response to phenylephrine or relaxation in response to {alpha}1-adrenoceptor antagonists on maximal sustained contraction induced by phenylephrine were constructed from control vessels and vessels pretreated with 100 µmol/l chloroethylclonidine (CEC) for 30 min. The significant decrease in the phenylephrine potency observed after CEC treatment together with the inhibitory potency displayed by 8-{2-[4-(2-methoxyphenyl)-1-piperazinyl]-8-azaspiro (4,5) decane-7-dionedihydrochloride} (BMY-7378, an {alpha}1D-adrenoceptor antagonist) confirm the relevant role of {alpha}1D-adrenoceptors in aorta and iliac and proximal mesenteric arteries. The potency of 5-methylurapidil (an {alpha}1A-adrenoceptor antagonist) and the changes in the potency of both BMY-7378 and 5-methylurapidil after CEC treatment provided evidence of a mixed population of {alpha}1A- and {alpha}1D-adrenoceptors in iliac and distal mesenteric arteries. The low potency of prazosin (pIC50 < 9) as well as the high 5-methylurapidil potency in tail and small mesenteric arteries suggest the main role of {alpha}1A/{alpha}1L-adrenoceptors with minor participation of the {alpha}1D-subtype. The mRNA levels and CEC treatment corroborated this pattern and confirmed that the {alpha}1L-adrenoceptor could be a functional isoform of the {alpha}1A-subtype.

chloroethylclonidine; prazosin; mesenteric arteries; adrenergic response


Address for reprint requests and other correspondence: P. D'Ocon, Departamento de Farmacología, Facultat de Farmàcia, Universitat de València, Avda, Vicent Andrés Estelles s/n, Burjassot, 46100 València, Spain (E-mail: m.pilar.docon{at}uv.es)




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