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Two prostaglandin endoperoxides, i. e. PGG2 and PGH2 were detected and isolated. They were unstable in aqueous medium (t1/2 at 37 degrees C about 5 min) and were converted to PGF2alpha by mild reducing agents. Human platelets as well as guinea pig lung and spleen converted the endoperoxides into thromboxane A2, an unstable (t1/2 at 37 degrees C about 30 s) oxetane/oxane derivative. Thromboxane A2 was converted into a stable hemiacetal derivative, thromboxane B2, by addition of 1 H2O. The two prostaglandin endoperoxides as well as thromboxane A2 caused platelet aggregation and the platelet release reaction. In addition they were potent stimulators of vascular and airway smooth muscle in vitro and in vivo.

The effect of various prostaglandins (PGs) and a thromboxane A2 (TXA2)-generating system on the contractility of rabbit splenic capsular smooth muscle has been investigated. PGI2 as well as higher concentrations of PGE1 and 5, 6 beta-dihydro-PGI2 inhibit noradrenaline-induced contractions of the smooth muscle preparation. The TXA2-generating system and high concentrations of PGD2, on the other hand, increase the contractions. The results support the concept that the hypothetical PGI2 receptor on the smooth muscle of the rabbit splenic capsule resembles, in its specificity, the PGI2 receptor on platelets.

The conversion of PGG2 to 15-hydroperoxythromboxane A2 by purified thromboxane synthase from human platelets was recently reported (Hammarström, S. (1980) J. Biol. Chem.255, 518). The hydroperoxythromboxane is approximately 25 times more potent than PGG2 in causing aggregation of human platelet rich plasma and 30 times more potent than PGG2 as an inducer of contractions of rabbit aorta.