Ishizawa M
Arch Int Pharmacodyn Ther. 1981 Sep;253(1):80-9.
A stable degradation product of prostacyclin (PGI2), 6-oxo-PGF1 alpha, and prostaglandin E2 (PGE2) were released from the smooth muscles of guinea-pig antrum into a bath solution in concentrations of 32.1 +2.5ng/g tissue/60 min (n=20) and 21.6 +2.3ng/g tissue/60 min (n=20), respectively. Stable PGI2 analog, PGI2 methylester (PGI2 m.e. 3x10(-11)-3x10(-6)M) and PGE2(3x10(-11)-3x10(-6)M) produced contraction of longitudinal muscle and inhibition of spontaneous phasic contractions of circular muscle. The actions of 6-oxo-PGF1 alpha (3x10(9)-3x10(-6)M) on both muscles were 100-1000-fold weaker than those of PGI2 m.e. In electrical activities recorded by the sucrose gap method, PGI2 m.e. (10(-6)M) depolarized the membrane and generated spike discharges on the slow wave of longitudinal muscle, and decreased spike discharges on the slow wave of circular muscle. These actions of PGI2 m.e. on both muscles, however, were 10-50-fold weaker than those of PGE2. The results suggest that prostacyclin does not play a main physiological role in the regulation of gastric motility in the guinea-pig.
