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This Article Full Text Full Text (PDF) All Versions of this Article: 288/5/H2439    most recent 00548.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Donoso, M. V. Articles by Huidobro-Toro, J. P. Search for Related Content PubMed PubMed Citation Articles by Donoso, M. V. Articles by Huidobro-Toro, J. P.

A_2B adenosine receptor mediates human chorionic vasoconstriction and signals through arachidonic acid cascade

Centro de Regulación Celular y Patología Prof. J. V. Luco, Instituto Milenio de Biología Fundamental y Aplicada, Departamento de Fisiología, Unidad de Regulación Neurohumoral, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile

Submitted 10 June 2004 ; accepted in final form 4 January 2005

Because adenosine is a vascular tone modulator, we examined the effect of adenosine and congeners in the vascular reactivity of isolated human placental vessels and in perfused cotyledons. We characterized its vasomotor action and tentatively identified the receptor subtypes and their intracellular signaling mechanisms. We recorded isometric tension from the circular layer of chorionic vessel rings maintained under 1.5 g of basal tension or precontracted with KCl. The relative order of potency of adenosine and structural analogs is consistent with the expression of A_2B receptors, 5'-(N-ethylcarboxamido)adenosine (NECA) being the most potent. The maximal contraction ranged from 45% to 60% of the KCl standard response, except for an A_2A receptor agonist that did not exceed 15%. Consistently, NECA was 100-fold more potent than adenosine to raise the perfusion pressure of ex vivo perfused cotyledons. In contrast, a selective A₃ receptor agonist relaxed precontracted rings of chorionic vessels. Whereas a selective A₃ receptor antagonist was ineffective to antagonize adenosine-induced contraction, A₂ or A₁ receptor antagonists reduced adenosine-induced vasoconstriction concentration-dependently. Denudation of the endothelial layer reduced adenosine- and NECA-induced contractions by 50–70%. Furthermore, indomethacin reduced adenosine- or NECA-induced contractions concentration-dependently in intact and endothelium-denuded rings. A thromboxane receptor antagonist blocked adenosine- and NECA-induced contractions in intact and endothelium-denuded rings, suggesting the involvement of an arachidonic acid metabolite as the mediator of the vasoconstriction. We propose that adenosine A_2B receptors mediate the adenosine-induced contraction vasomotor effect in human chorionic vessels and that this involves synthesis of a thromboxane receptor activator or a related prostanoid.

adenosine-induced vasoconstriction; human chorionic vessels; arachidonate metabolite; thromboxane receptor antagonism; placental vasculature

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