Related Experiment Video
Updated: Jul 31, 2026

Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
Published on: April 6, 2017
Adenosine diphosphate-induced platelet activation inhibited by magnesium in a dose-dependent manner
W L Leaphart1, M C Meyer, E L Capeless
1Department of Biochemistry, University of Vermont, Burlington, USA.
Objective:
To examine the hypothesis that magnesium inhibits platelet activation at concentrations equivalent to therapeutic levels.
Methods:
Fifteen subjects were enrolled: five healthy, female donors with regular, spontaneous menstrual cycles; five women with uncomplicated third-trimester pregnancies; and five preeclamptic subjects before magnesium therapy. Anticoagulated whole blood was added to tubes containing 0.5 micromol/L adenosine diphosphate (to activate platelets), HP1-1D (activation-independent platelet antibody), CD62 antibody and CD63 antibody (activation-dependent platelet antibodies), and magnesium sulfate in increasing concentrations (2-100 mg/dL). The percentage of activated platelets (CD62 or CD63 positive) was determined using three-color flow cytometric analysis. Data were analyzed using the Student t test, repeated measures analysis of variance, two-way analysis of variance, and Student-Newman-Keuls for pairwise comparison in appropriate cases. P < .05 was considered significant.
Results:
Adenosine diphosphate-induced platelet activation was inhibited with increasing magnesium concentration in all subjects (P < .001). Significant inhibition of CD62 and CD63 expression first occurred at a magnesium concentration of 4 mg/dL in the normal pregnant group (P < .05), at 6 mg/dL in the preeclamptic group (P < .05), and at 8 mg/dL in the nonpregnant group (P < .05).
Conclusion:
Magnesium inhibits adenosine diphosphate-induced platelet activation in a dose-dependent manner. This effect initially attains statistical significance at concentrations equivalent to therapeutic levels.
Related Concept Videos
Calmodulin-dependent Signaling
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Antihypertensive Drugs: Action of Calcium Channel Blockers
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Formation of the Platelet Plug
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...

