We investigated the eicosanoid synthesis of platelets of Wistar and of Okamoto spontaneously hypertensive rats (SHR), and the effect of captopril in vitro, using [14C]arachidonic acid as a tracer substrate and chromatographic determination. Lipoxygenase activity was elevated, while the formation of cyclooxygenase products was reduced in SHR platelets, compared to those of Wistar rats. This difference might play a role in the pathomechanism of hypertension in SHR. In SHR with lower blood pressure, captopril reduced thromboxane synthesis, while in SHR with higher blood pressure thromboxane synthesis was unchanged, but the synthesis of prostaglandin D2, a potent vasodilator, and of 12-L-hydroxy-5,8,10-heptadecatrienoic acid, a stimulator of endothelial prostacyclin formation, was increased. We may conclude that, in spite of the missing angiotensin converting enzyme in platelets, a direct effect on platelet eicosanoid synthesis could contribute to the blood pressure decreasing effect of captopril.