Biochemistry of Platelets by David R. Phillips

By David R. Phillips

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1981). The elevation of cAMP induced by P G I , PGEj, or P G D occurs rapidly, reaches its peak between 20 and 60 seconds, and then decreases gradually. This decline is abolished in the presence of phosphodiesterase inhibitors. These observations, together with the finding that cAMP phosphodiesterase activity increases in platelets preincubated with P G I , led Alvarez et al. (1981) to postulate that these prostaglandins cause a sequential activation of adenylate cyclase and cAMP phosphodiesterase.

Diacylglycerol alone, however, is insufficient to account for signal transduction in platelets. , 1983), which did not cause aggregation or secretion by themselves, led to full activation when added together. Similarly, in platelets made permeable to CaEGTA by high voltage electric discharge (Knight and Scrutton, 1984), either OAG or 12-0-tetradecanoylphorbol 13-acetate (TPA) enhanced the C a + -sensitivity of the secretory process. These experiments were interpreted as evidence of the synergistic action of two intracellular second messengers, diacylglycerol and calcium.

B. Inositol Trisphosphate Inositol trisphosphate has been proposed as the link between receptor activa­ tion and calcium mobilization, because it can induce the release of calcium from a nonmitochrondrial intracellular source from a variety of cells permeabilized by various techniques (reviewed by Berridge and Irvine, 1984). The mobilization of calcium by inositol trisphosphate is quite specific, since other related com­ pounds, such as myoinositol, inositol phosphate, inositol bisphosphate, and in­ ositol cyclic phosphate, are ineffective (Streb et aL, 1983; Berridge and Irvine, 1984).

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