Abstract
In the vessel wall arachidonic acid, the major precursor of eicosanoid biosynthesis in mammalian tissues, is mainly metabolized via the cyclo-oxygenase pathway. In the endothelial or smooth muscle layers of the blood vessel wall, arachidonic acid is preferentially converted to prostaglandin (PG)I2, which is a potent vasodilator and inhibitor of platelet aggregation [32]. In blood platelets, on the other hand, arachidonic acid is preferentially converted via cyclo-oxygenase and thromboxane (TX) synthetase to TXA2, a vasoconstrictor and potent inducer of platelet aggregation [22]. On the basis of these facts a TXA2-PGI2 balance had been proposed, offering a concept for the participation of eicosanoids in normal hemostasis and in pathological conditions [32]. This hypothesis has stimulated an abundance of basic and clinical research, even though the importance of PGI2 has recently been questioned [26].
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© 1987 Springer-Verlag, Berlin Heidelberg
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Simmet, T., Peskar, B.A. (1987). Profile of Generation of Eicosanoids by Blood Vessels and the Heart. In: Gryglewski, R.J., Stock, G. (eds) Prostacyclin and Its Stable Analogue Iloprost. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-71499-3_14
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