Helically cut femoral artery strips from humans (bypass surgery), dogs and rabbit were set up for isometric recording. The endothelial layer was removed by rubbiing, hence the vascular strips used in this study are considered to be arterial smooth muscle preparations without endothelium. The indomethacin-, prostaglandin F(2α)- and PGI2-induced changes in tone were determined. Indomethacin (3 μmol/l) potentiated the contractile responses of human and canine vessels to PGF(2α0 by 60.0±10.4 and 108±12%, respectively. By contrast, the PGF(2α)-induced contractions of rabbit arteries were not enhanced by the cyclooxygenase inhibitor. PGI2 diminished the tone of the PGF(2α)-contracted vessels obtained from all the three species in a concentration-related manner. The potency of the relaxant prostanoid differed, however, markedly (p<0.02) from species to species. The IC50 values (molar concentrations of PGI2 producing 50 percent reduction in the PGF(2α)-induced tone) were 20.8±1.9, 133±24 and 286±52 nmol/l for human, dog and rabbit arteries, respectively. The results clearly demonstrate a significant interspecies difference in the prostacyclin-sensitivity of the blood vessels studied. The differential responsiveness to indomethacin may reflect species-difference in the regulatory function of PGI2 in arterial smooth muscle tone.
|Journal||Biomedica Biochimica Acta|
|Publication status||Published - Jan 1 1988|
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