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.