Effects of dipyridamole, nifedipine, verapamil, hydralazine and propranolol on the formation of prostacyclin and thromboxane in a coupled system of platelets and aorta

Verapamil Reduces Intimal Hyperplasia in a Sheep Carotid Artery Patch Graft Model

“…17 It has been reported that calcium antagonists can inhibit aggregation of human platelets in the presence of ADP, adrenaline, collagen, or arachidonate. 18 Such a mechanism would reduce the amount of PDGF entering the artery wall and therefore reduce IH development. Platelet accumulation occurs in a rapid and time‐dependent manner, 19 with platelet adherence beginning within minutes and persisting for hours.…”

Effects of nilvadipine, a calcium antagonist, on intimal thickness of vascular grafting in cholesterol-fed rabbits

“…Platelets are also considered to be an important mediator of detrimental events in graft failure, i.e., thrombogenesis, progressive intimal hyperplasia, and atherogenesis [28]. Srivastava [29] reported the ability of nifedipine, verapamil, and hydralazine to inhibit aggregation of human platelets in the presence of ADP, epinephrine, collagen, or arachidonate. Therefore, one might speculate that calcium antagonists reduce intimal thickness by inhibiting platelet aggregation stimulated by collagen exposed in the subendothelium after endotherial injury.…”

Nifedipine Increases Urinary Excretion of Prostacyclin Metabolite in Hypertensive Pregnancy

“…An enhancement of 6-keto-PGFI, excretion by nifedipine found in the present study suggests correction of this imbalance between TXA, and PGI, in kidney. Nifedipine enhances PGI, formation also in rat lungs (Srivastava & Awasthi 1983) and in a coupled system of human platelets and rat aorta by unknown mechanism (Srivastava 1986). However, nifedipine (40 mg orally) does not increase 6-keto-PGF,, in plasma in normotensive subjects (Murphy et af.…”