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This Article Full Text Full Text (PDF) All Versions of this Article: 573/2/427    most recent jphysiol.2006.105882v1 Services Email this article to a friend Similar articles in this journal 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 Google Scholar Google Scholar Articles by Buvinic, S. Articles by Huidobro-Toro, J. P. Search for Related Content PubMed PubMed Citation Articles by Buvinic, S. Articles by Huidobro-Toro, J. P. Related Collections Cardiovascular

¹ Centro de Regulación Celular y Patología J.V. Luco, Instituto Milenio de Biología Fundamental y Aplicada MIFAB, Departamento de Fisiología, Facultad de Ciencias Biológicas, P. Universidad Católica de Chile, Santiago, Chile

The expression of purinergic P2Y receptors (P2YRs) along the cord, superficial chorionic vessels and cotyledons of the human placenta was analysed and functional assays were performed to determine their vasomotor activity. Immunoblots for the P2Y₁R and P2Y₂R revealed a 6- to 8-fold increase in receptor expression from the cord to the chorionic or cotyledon vessels. In the cord and chorionic vessels the receptor distribution was mainly in the smooth muscle, whereas in the cotyledon vessels these receptors were equally distributed between the endothelium and smooth muscle cells. An exception was the P2Y₂R at the umbilical artery, which was distributed as in the cotyledon. mRNA coding for the P2Y₁R and P2Y₂R were detected by RT-PCR and the mRNA coding for the P2Y₄R, P2Y₆R and P2Y₁₁R was also identified. Application of 2-MeSADP and uridine triphosphate (UTP), preferential P2Y₁R and P2Y₂R ligands, respectively, resulted in contraction of isolated rings from umbilical and chorionic vessels. The vasoconstriction was blocked in a concentration-dependent manner by 10–100 nM indomethacin or 10 nM GR32191, suggesting the involvement of thromboxane receptors. MRS 2179, a selective P2Y₁R antagonist, reduced the 2-MeSADP- but not the UTP-evoked contractions. Perfusion of cotyledons with 2-MeSADP or UTP evoked concentration-dependent reductions in perfusion pressure mediated by the NO–cGMP pathway. Blockade of NO synthase abolished the vasodilatation and the rise in luminal NO elicited by either agonist. MRS 2179 antagonized the dilatation and rise in luminal NO evoked by 2-MeSADP but not by UTP. In summary, P2Y₁R and P2Y₂R are unevenly distributed along the human placental vascular tree; both receptors are coupled to different signalling pathways in the cord/chorionic vessels versus the cotyledon leading to opposing vasomotor responses.

(Received 22 January 2006; accepted after revision 15 March 2006; first published online 16 March 2006)
Corresponding author J. Pablo Huidobro-Toro: Dept. of physiology, Faculty of Biological Science, P. Catholic University of Chile, PO Box 114-D, Santiago 1, Chile. Email: jphuid{at}bio.puc.cl

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