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Identification of a prostanoid FP receptor population producing endothelium‐dependent vasorelaxation in the rabbit jugular vein
Author(s) -
Chen J.,
ChampaRodriguez M.L.,
Woodward D.F.
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb15960.x
Subject(s) - prostanoid , rabbit (cipher) , receptor , population , endothelium , jugular vein , vein , endocrinology , anatomy , biology , medicine , chemistry , computer science , environmental health , computer security
1 Prostaglandin F 2α (PGF 2α ) and its synthetic analogue, fluprostenol, potently relaxed the precontracted isolated jugular vein of the rabbit (RJuV). The vasorelaxant activity of PGF 2α and fluprostenol was dependent upon an intact vascular endothelium. Although removal of the vascular endothelium abolished activity associated with PGF 2α ‐like agonists, it did not significantly alter the relaxant effects of prostaglandin E 2 (PGE 2 ). 2 The nitric oxide synthase inhibitor, N G ‐nitro‐L‐arginine methyl ester ( l ‐NAME), at 100 μ m significantly inhibited the endothelium‐dependent relaxations induced by PGF 2α . Lower doses (1 μ m , 10 μ m ) of l ‐NAME had little or no effect. The relaxant effects of PGE 2 were not affected by l ‐NAME (1–100 μ m ). D‐NAME at 100 μ m was without effect on the vasorelaxant responses to either PGF 2α or PGE 2 . 3 The potassium (K)‐channel blockers tetraethylammonium (TEA, 1 m m ), barium (1 m m ) and quinine (100 μ m ), each tested in the presence of the inactive enantiomer D‐NAME (100 μ m ) did not significantly affect the response to PGF 2α . Unexpectedly, both TEA and barium significantly and partially reversed the inhibitory effects of 100 μ m l ‐NAME, whereas quinine had no effect. In similar studies, none of the three potassium channel blockers had any effect on relaxations elicited by PGE 2 when given with D‐NAME or l ‐NAME. 4 These results indicate that the PGF 2α ‐sensitive prostanoid receptors found in the vascular endothelium of the rabbit jugular vein are of the FP‐receptor subtype. Nitric oxide (NO) appears to be the predominant messenger involved in PGF 2α ‐induced relaxation of the rabbit jugular vein. Potassium channels may have a minor role in mediating the vasorelaxation response to PGF 2α . When both NO synthesis and K‐channels are simultaneously blocked, inhibition of PGF 2α ‐induced vasorelaxation by l ‐NAME is opposed by K‐channel blockers. This diminution of the inhibitory effect of l ‐NAME by TEA and barium suggests that K‐channels may possibly serve a compensatory role via the NO pathway.