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Titolo:
Antiplatelet action of losartan involves TXA(2) receptor antagonism but not TXA(2) synthase inhibition
Autore:
Chlopicki, S; Koda, M; Chabielska, E; Buczko, W; Gryglewski, RJ;
Indirizzi:
Jagiellonian Univ, Dept Pharmacol, Coll Med, PL-31531 Krakow, Poland Jagiellonian Univ Krakow Poland PL-31531 ll Med, PL-31531 Krakow, Poland Med Acad Bialystok, Dept Pharmacodynam, Bialystok, Poland Med Acad Bialystok Bialystok Poland pt Pharmacodynam, Bialystok, Poland
Titolo Testata:
JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
fascicolo: 4, volume: 51, anno: 2000,
parte:, 1
pagine: 715 - 722
SICI:
0867-5910(200012)51:4<715:AAOLIT>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANGIOTENSIN-II RECEPTORS; PLATELET-AGGREGATION; PATHO-PHYSIOLOGY; DUP-753;
Keywords:
platelets; AT(1) antagonists; TP receptors; TXA(2) synthase; imidazole;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Chlopicki, S Jagiellonian Univ, Dept Pharmacol, Coll Med, Grzegorzecka 16,PL-31531 Krakow, Poland Jagiellonian Univ Grzegorzecka 16 Krakow Poland PL-31531 and
Citazione:
S. Chlopicki et al., "Antiplatelet action of losartan involves TXA(2) receptor antagonism but not TXA(2) synthase inhibition", J PHYSL PH, 51(4), 2000, pp. 715-722

Abstract

Various AT(1) receptor antagonists including losartan are known to inhibithuman platelet activation by antagonising TXA(2)/PGH(2) receptors (TP receptors). Presently, we check a hypothesis that losartan, an imidazole derivative in contrast with valsartan, a non-imidazole compound, may inhibit human platelet activation also through inhibition of TXA(2) synthesis. Inhibitory action of losartan (2-n butyl-4-chloro-5-hydroxymethyl-1-beta (2'-(1H-tetrazol-5yl)biphenyl-4-yl)methyl] imidazole), its active metabolite EXP 3174(2-n-butyl-4-chloro-1-beta (2-(1H-tetrazol-5-yl) biphenyl-4-yl) methyl]imidazole-5-carboxylic acid) and valsartan ((S)-N-valeryl-N-(beta2'-(1H-tetrazol-5-yl)biphenyl-4-yl]methyl]valine), on collagen-induced platelet aggregation and TXA(2) generation was compared to effects achieved by each compoundon U46619-induced aggregation in aspirinized platelets. Losartan and aspirin inhibited collagen-induced platelet aggregation with approximately the same potency, whereas EXP 3174 and valsartan showed much weaker antiplateleteffects. Interestingly, losartan, EXP 3174 and valsartan displayed similarpotencies as inhibitors of U46619-induced aggregation in asprinized platelets as in collagen-induced aggregation in non-aspirinized platelets. None of the above three AT antagonists, up to concentration of 300 muM, did influence collagen-induced TXA(2) synthesis in human platelets. In conclusion, antiplatelet effects of AT antagonists, irrespective of the presence or absence of non-condensed imidazole in their chemical structure, involve antagonism of TP receptors but not inhibition of TXA(2) synthesis in platelets.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 12:49:24