By David R. Phillips
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Additional resources for Biochemistry of Platelets
The fact that 8-bromo cGMP can inhibit platelet functions also indicates that cGMP, as well as cAMP, is inhibitory. Takai et al. (1981b) reported that nitroprusside caused a rise in cGMP levels and a concomitant inhibition of production of diacyglycerol, phosphorylation of 40K protein, and secretion of serotonin in thrombin-stimulated platelets. These effects were accompanied by enhanced phosphorylation of a 50K protein. 8Bromo cGMP had a similar effect. Since dibutyryl cAMP also inhibits these platelet functions as well as stimulating phosphorylation of the 50K and other proteins, Takai et al.
Change in Intracellular pH A variety of cell functions have been shown to correlate with changes in intracellular pH (for background see proceedings of a symposium edited by Nuccitelli and Deamer, 1982), and Home et al. (1981) reported that thrombin caused an increase in platelet cytosolic pH, measured with fluorescent probes. The dose dependence and the time course of the change were consistent with a role in stimulus-response coupling, but the important cause-effect relationship has not been established nor have changes in response to other agonists been reported.
Decreased Levels of Cyclic AMP in Response to Platelet Stimulation Since elevated levels of cAMP inhibit platelet activation, does a reduction in the level of cAMP cause activation? , 1977; Haslam and Vanderwal, 1982), and ADP, epinephrine, thrombin, and PAF have been shown to inhibit adenylate cyclase activity in cell-free preparations (Cooper and Rodbell, 1979; Steer and Wood, 1979; Haslam and Vanderwal, 1982; Aktories and Jakobs, 1984). Other platelet agonists, such as vasopressin and the endoperoxide analogs U-46619 and U44069, however, can activate platelets but are unable to lower the elevated levels of cAMP (Haslam, 1975; Best et al, 1979), indicating that supression of cAMP levels is not a prerequisite for platelet activation.
Biochemistry of Platelets by David R. Phillips