Effect of Concanavalin A on Serotonin Transport into Blood Platelets: Possible Involvement of Protein Kinase C

Effect of Concanavalin A on Intracellular Calcium Concentration in Single Blood Platelets

“…Thus, Con A in duced elevation of [Ca+ +]i was suggested to consist of two different kinds of processes, namely mobilization of Ca++ from the in tracellular storage sites and successive Ca++ influx through Ca++ channels. The latter effect of Con A was already described in the experiment using 45Ca+ + as a tracer (8). The same effect of Con A on Ca++ channels was also reported with lymphocytes (20), spleen cells (21) and mast cells (22).…”

“…Effect of Con A on serotonin transport into blood platelets in the presence of EGTA As already reported in our previous papers (4,8), Con A was shown to have a potent in hibitory effect on the transport of 5-HT into blood platelets without a 5-HT release reac tion. This inhibitory effect of Con A, how ever, was not affected by EGTA.…”

“…It is suggested that the effect of Con A on 5-HT transport might be exerted through Ca++ mobilization from its intracellu lar storage sites. Then, as suggested in our previous paper, protein kinase C might be subsequently activated to inhibit 5-HT trans port (8). The phosphorylation of a 40-kDa platelet protein was also demonstrated by Con A treatment through the activation of protein kinase C (8).…”

“…Assay of serotonin transport into blood platelets Determination of 5-HT transport into platelets was performed by the previously de scribed method (8). Briefly, aliquots (1 ml) of diluted PRP were pre-incubated with or with out drug in the presence of heparin (10 units/ml) at 37°C.…”

“…Fredholm and Dunwiddie (7) has sug gested that adenosine may depress transmitter release in several ways, including inhibition of adenylate cyclase, opening K+ channels and reduction of Ca+ + influx. It has also been speculated that c-AMP may interrupt IP3 formation/Ca++ release/protein kinase C pathway through a mechanism in which pro tein kinase A activation is involved (8). The idea that the activation of protein kinase C ex ert a regulatory role on adenylate cyclase was also suggested in many cell systems (9-11) in cluding human platelets (12).…”