Related Experiment Video
Updated: Oct 2, 2026

Real-time Evaluation of Absolute, Cytosolic, Free Ca2+ and Corresponding Contractility in Isolated, Pressurized Lymph Vessels
Published on: March 22, 2024
Antiplatelet Effect of Nifedipine depending on its Action on Red Cell Deformability in Essential Hypertension
Sergey E. Akopov1, Movses A. Sarkisian
1Department of Pharmacology, Yerevan Medical Institute, 375025 Yerevan, Armenia.
In patients with essential hypertension, increased level of platelet activity expressed as the concentrations of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were observed. Elevation of the levels of both beta-TG and PF4 correlated with the increase in platelet aggregability in platelet-rich plasma (PRP) and the decrease in red blood cell deformability, which were considered as being the possible factors for the platelet intravascular activation. After 2 weeks of monotherapy with nifedipine (40 mg daily), a decrease in platelet aggregability in PRP was observed in 35 of the 75 patients and an increase in red cell deformability in 37 of the 75 patients. Using cluster analysis, all cases were divided into several groups based on nifedipine effects on red cell deformability and platelet aggregability in PRP. It was revealed that the statistically significant decrease in the levels of platelet markers took place only in patients in whom nifedipine simultaneously decreased platelet aggregability and increased red cell deformability. Analysis of variance showed a high power of influence for combined changes in these parameters for reducing intravascular platelet activation by nifedipine. It is suggested that nifedipine reduces platelet activity by direct action on platelets and indirectly due to its capacity to increase red cell deformability, resulting in elimination of platelet stimulation by red blood cells.
In patients with essential hypertension, increased level of platelet activity expressed as the concentrations of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were observed. Elevation of the levels of both beta-TG and PF4 correlated with the increase in platelet aggregability in platelet-rich plasma (PRP) and the decrease in red blood cell deformability, which were considered as being the possible factors for the platelet intravascular activation. After 2 weeks of monotherapy with nifedipine (40 mg daily), a decrease in platelet aggregability in PRP was observed in 35 of the 75 patients and an increase in red cell deformability in 37 of the 75 patients. Using cluster analysis, all cases were divided into several groups based on nifedipine effects on red cell deformability and platelet aggregability in PRP. It was revealed that the statistically significant decrease in the levels of platelet markers took place only in patients in whom nifedipine simultaneously decreased platelet aggregability and increased red cell deformability. Analysis of variance showed a high power of influence for combined changes in these parameters for reducing intravascular platelet activation by nifedipine. It is suggested that nifedipine reduces platelet activity by direct action on platelets and indirectly due to its capacity to increase red cell deformability, resulting in elimination of platelet stimulation by red blood cells.
Related Concept Videos
Antihypertensive Drugs: Vasodilators
Antihypertensive Drugs: Action of Calcium Channel Blockers
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...
Antianginal Drugs: Nitrates and β-Blockers
Organic nitrates, such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...
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...
