NIFEDIPINE REDUCES THROMBOXANE A(2) PRODUCTION BY PLATELETS WITHOUT CHANGING AGGREGATION IN HYPERTENSIVE PREGNANCY

Authors
Citation
A. Manninen, NIFEDIPINE REDUCES THROMBOXANE A(2) PRODUCTION BY PLATELETS WITHOUT CHANGING AGGREGATION IN HYPERTENSIVE PREGNANCY, Pharmacology & toxicology, 78(6), 1996, pp. 387-391
Citations number
26
Categorie Soggetti
Pharmacology & Pharmacy",Toxicology
Journal title
ISSN journal
09019928
Volume
78
Issue
6
Year of publication
1996
Pages
387 - 391
Database
ISI
SICI code
0901-9928(1996)78:6<387:NRTAPB>2.0.ZU;2-A
Abstract
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.