[Biochemical features of platelet alpha2-adrenergic receptors and their connection with an increase in concentration of intracellular Ca2+].

Epinephrine (E) and norepinephrine (NE) alone did not increase free intracellular Ca2+ ([Ca2+]i) in human platelets loaded with Quin-2 or Fura-2; however, they did potentiate the effects of vasopressin (VP), serotonin (S) and platelet activating factor (PAF). The synergism in [Ca2+]i increase was also obtained in the presence of VP together with PAF, S with PAF as well as VP with S. The effect of E or NE was blocked by yohimbine and phentolamine. Prazosin was less effective, while propranolol had no effect at all. Clonidine did not potentiate the effects of VP, S or PAF on [Ca2+]i; however, it did block the potentiation induced by E or NE. E potentiated the VP-induced 45Ca2+ uptake as well as VP-stimulated inositol 1,4,5-trisphosphate (IP3) formation. E alone did not change significantly the level of IP3 in platelets, nor did it influence the cyclic AMP level. The experimental results suggest that both Ca2+ influx and polyphosphoinositide breakdown underlie the mechanism of potentiation.