Owen N E, Feinberg H, Le Breton G C
Am J Physiol. 1980 Oct;239(4):H483-H488. doi: 10.1152/ajpheart.1980.239.4.H483.
Human blood platelets isolated by albumin density gradient centrifugation take up Ca2+ during 10(-6)M epinephrine-induced primary aggregation but not during 10(-6)M ADP-induced primary aggregation. Platelet uptake of Ca2+ is dose-dependent over a range of 10(-7) to 10(-5) M epinephrine. Antagonism of the platelet alpha-receptor by phentolamine (10(-6)M) results in inhibition of both epinephrine-stimulated Ca2+ uptake and aggregation. The Ca2+ antagonist verapamil (50 micro M) blocks Ca2+ uptake and epinephrine-induced aggregation, but not ADP-induced aggregation. The verapamil inhibition of aggregation is reduced on Ca2+ addition. These results suggest that epinephrine acts to stimulate primary platelet aggregation through a specific receptor interaction that results in a selective increase in platelet membrane permeability to Ca2+.
通过白蛋白密度梯度离心分离的人血小板在10⁻⁶M肾上腺素诱导的初级聚集过程中摄取Ca²⁺,但在10⁻⁶M ADP诱导的初级聚集过程中不摄取。在10⁻⁷至10⁻⁵M肾上腺素范围内,血小板对Ca²⁺的摄取呈剂量依赖性。酚妥拉明(10⁻⁶M)对血小板α受体的拮抗作用导致肾上腺素刺激的Ca²⁺摄取和聚集均受到抑制。Ca²⁺拮抗剂维拉帕米(50μM)阻断Ca²⁺摄取和肾上腺素诱导的聚集,但不阻断ADP诱导的聚集。添加Ca²⁺后,维拉帕米对聚集的抑制作用减弱。这些结果表明,肾上腺素通过特定的受体相互作用刺激血小板初级聚集,导致血小板膜对Ca²⁺的通透性选择性增加。