Prostanoid receptors involved in the relaxation of human pulmonary vessels

Citation
L. Walch et al., Prostanoid receptors involved in the relaxation of human pulmonary vessels, BR J PHARM, 126(4), 1999, pp. 859-866
Citations number
44
Categorie Soggetti
Pharmacology & Toxicology
Journal title
BRITISH JOURNAL OF PHARMACOLOGY
ISSN journal
00071188 → ACNP
Volume
126
Issue
4
Year of publication
1999
Pages
859 - 866
Database
ISI
SICI code
0007-1188(199902)126:4<859:PRIITR>2.0.ZU;2-7
Abstract
1 To characterize the prostanoid receptors on human pulmonary smooth muscle involved in vasodilatations, isolated arteries and veins were contracted w ith norepinephrine (10 mu M) and vessels were subsequently challenged with different prostanoid-receptor agonists in the absence or presence of select ive antagonists. 2 Prostaglandin D-2 (PGD(2)) and the selective DP-receptor agonist, BW245C, induced relaxations in the contracted human pulmonary venous preparations. The pot values were: 6.88 +/- 0.11 (n = 17) and 7.31+/-0.12 (n=5), respect ively. The relaxant responses induced by PGD, were reduced by the selective DP-receptor antagonist, BWA868C, and the estimated pA(2) value was 7.84+/- 0.16 (n=4). PGD(2) and BW245C did not relax contracted human pulmonary arte ries. 3 The selective IF-receptor agonists, iloprost and cicaprost, both induced relaxations in the contracted human vascular preparations. The pD(2) values for iloprost were: 7.84+/-0.08 (n=6) and 8.25+/-0.06 (n=4) and for cicapro st: 8.06+/-0.12 (n=5) and 8.11+/-0.09 (n=5) in arteries and veins respectiv ely. 4 Prostaglandin E-2 (PGE(2)) and the EP2/EP3-receptor agonist, misoprostol, partially relaxed the contracted venous preparations and the pD(2) values were: 8.10+/-0.15 (n = 15) and 6.24 +/- 0.33 (n = 3), respectively. These r elaxations suggest the presence of an EP receptor in the human pulmonary ve ins. The contracted human pulmonary arteries did not relax when challenged with PGE(2). 5 In human pulmonary venous preparations, the PGR-induced relaxations were neither modified by treatment with TP/EP4-receptor antagonist, AH23848B (10 and 30 mu M, n=6), nor by the DP/EP1/EP2-receptor antagonist, AH6809 (3 mu M, n=6). 6 These data suggest that the relaxation induced by prostanoids involved DP -, IP-receptors and to a lesser extent an EP-receptor on human pulmonary ve nous smooth muscle. In contrast, only the IP-receptor is involved in the pr ostanoid induced relaxations on human pulmonary arterial smooth muscle.