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Am J Physiol Heart Circ Physiol 280: H2342-H2349, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 5, H2342-H2349, May 2001

Characterization of PGE2 receptors in fetal and newborn lamb ductus arteriosus

Asmàa Bouayad1,*, Hiroki Kajino3,*, Nahid Waleh3, Jean-Claude Fouron1, Gregor Andelfinger1, Daya R. Varma2, Amanda Skoll1, Alejandro Vazquez1, Fernand Gobeil Jr1, Ronald I. Clyman3, and Sylvain Chemtob1,2

1 Departments of Cardiology, Pediatrics, and Physiology, Université de Montréal, Quebec H3T 1C5; 2 Departments of Pharmacology and Therapeutics, McGill University, Quebec, Canada H3G 1Y6; and 3 Cardiovascular Research Institute and Department of Pediatrics, University of California San Francisco, San Francisco, California 94143

Although the role of PGE2 in maintaining ductus arteriosus (DA) patency is well established, the specific PGE2 receptor subtype(s) (EP) involved have not been clearly identified. We used late gestation fetal and neonatal lambs to study developmental regulation of EP receptors. In the fetal DA, radioligand binding and RT-PCR assays virtually failed to detect EP1 but detected EP2, EP3D, and EP4 receptors in equivalent proportions. In the newborn lamb, DA total density was one-third of that found in the fetus and only EP2 was detected. Stimulation of EP2 and EP4 increased cAMP formation and was associated with DA relaxation. Though stimulation of EP3 inhibited cAMP formation, it surprisingly relaxed the fetal DA both in vitro and in vivo. This EP3-induced relaxation was specifically diminished by the ATP-sensitive K+ (KATP) channel blocker glibenclamide. In conclusion, PGE2 dilates the late gestation fetal DA through pathways that involve either cAMP (EP2 and EP4) or KATP channels (EP3). The loss of EP3 and EP4 receptors in the newborn DA is consistent with its decreased responsiveness to PGE2.

ductus arteriosus; EP receptors; ATP-sensitive potassium channels.

* A. Bouayad and H. Kajino have equally contributed to this work.




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