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- Title
Prostacyclin release and receptor activation: differential control of human pulmonary venous and arterial tone.
- Authors
Norel, Xavier; Walch, Laurence; Gascard, Jean-Pierre; de Montpreville, Vincent; Brink, Charles
- Abstract
1: In human pulmonary vascular preparations, precontracted arteries were more sensitive to the relaxant effect of acetylcholine (ACh) than veins (pD2 values: 7.25±0.08 (n=23) and 5.92±0.09 (n=25), respectively). Therefore, the role of prostacyclin (PGI2) was explored to examine whether this mediator may be responsible for the difference in relaxation. 2: In the presence of the cyclooxygenase (COX) inhibitor, indomethacin (INDO), the ACh relaxations were reduced in arteries but not in veins. On the contrary, an inhibitor (L-NOARG) of the nitric oxide synthase blocked preferentially the relaxation in veins. 3: A greater release of 6-keto-PGF1a, the stable metabolite of PGI2, was observed in arterial preparations than in venous preparations when stimulated with either ACh or arachidonic acid (AA). 4: Exogenous PGI2 produced a reduced relaxant effect in the precontracted vein when compared with the artery. In the presence of the EP1-receptor antagonist AH6809, the PGI2 relaxation of veins was similar to arteries. 5: In veins, AA (0.1?mM) produced a biphasic response, namely, a contraction peak (0.4-0.5?g) followed by a relaxation. These contractions in venous preparations were abolished either in the absence of endothelium or in the presence of INDO or an EP1-receptor antagonist (AH6809, SC19220). In the arterial preparations AA induced only relaxations. 6: In both vascular preparations, COX-1 but not the COX-2 protein was detected in microsomal preparations derived from homogenized tissues or freshly isolated endothelial cells. 7: The differential vasorelaxations induced by ACh may be explained, in part, by a more pronounced production and release of PGI2 in human pulmonary arteries than in the veins. In addition, while PGI2 induced relaxation by activation of IP-receptors in both types of vessels, a PGI2 constrictor effect was responsible for masking the relaxation in the veins by activation of the EP1-receptor.British Journal of Pharmacology (2004) 142, 788-796. doi:10.1038/sj.bjp.0705843
- Subjects
PULMONARY blood vessels; HEMODYNAMICS; PROSTACYCLIN; CYCLOOXYGENASES; ARACHIDONIC acid; BLOOD flow
- Publication
British Journal of Pharmacology, 2004, Vol 142, Issue 4, p788
- ISSN
0007-1188
- Publication type
Article
- DOI
10.1038/sj.bjp.0705843