A. Manninen, NIFEDIPINE REDUCES THROMBOXANE A(2) PRODUCTION BY PLATELETS WITHOUT CHANGING AGGREGATION IN HYPERTENSIVE PREGNANCY, Pharmacology & toxicology, 78(6), 1996, pp. 387-391
Platelet aggregation and thromboxane Al generation were studied in hyp
ertensive pregnant women using normotensive non-pregnant and pregnant
controls. In hypertensive pregnancy, adrenaline- and adenosine diphosp
hate-induced platelet aggregation was at the non-pregnant level and lo
wer than in normotensive pregnancy. Collagen-induced aggregation was a
t a lower level in hypertensive pregnancy than in both control groups.
Thromboxane generation during spontaneous clotting and in platelet-ri
ch plasma did not differ between the three groups. However, thromboxan
e generation was low during aggregation induced by small collagen conc
entrations in hypertensive pregnancy, but at higher collagen concentra
tions the difference between the groups disappeared. During nifedipine
treatment (10 mg t.i.d.), aggregation and thromboxane production in p
latelet-rich plasma induced by the three stimuli remained unaltered in
hypertensive pregnancy while thromboxane synthesis during spontaneous
clotting was reduced. In nifedipine-treated non-pregnant controls, on
ly EC(80) for adrenaline-induced aggregation decreased. In vivo, pharm
acological concentrations of nifedipine inhibited platelet aggregation
and thromboxane production. In conclusion, nifedipine reduces thrombo
xane generation in spontaneous clotting, without inhibiting platelet a
ggregation and thromboxane production in platelet-rich plasma in hyper
tensive pregnancy. Reduced aggregability of platelet ex vivo may refle
ct their continuous activation and desensitization in vivo in hyperten
sive pregnancy.