Captopril as a modifier of the arachidonate cascade of rat platelets

A. Gecse, G. Telegdy

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Abstract

The lipoxygenase pathway of arachidonate cascade in the platelets of spontaneously hypertensive rats has been found to be significantly higher than in normotensive animals. Repeated oral administration of Captopril (in drinking water - 200 mg/100 ml) for 14 days resulted in an elevation in the activity of arachidonate cascade in the platelets of treated rats. At the same time the Captopril treatment induced the formation of 12-hydroxy-heptadecatrienoic acid (12-HHT), which molecule is known to be a potent prostacyclin (PGI2) releaser and/or synthesis inducer. PGI2 is one of the most potent vasodilatator molecule in living organisms. The in vitro experiments in rat platelets suggest, that very low doses of Captopril (10-12 to 10-10 M) result in a significantly elevated 12-HHT synthesis. Captopril might act through the 12-HHT PGI2 mechanism, resulting in blood pressure reduction. The lipoxygenase pathway of platelets, the formation of 12-hydroxyeicosatetraenoic acid (12-HETE), was significantly elevated in vitro in the presence of low dose of Captocril (10-11 and 10-10).

Original languageEnglish
Pages (from-to)201-208
Number of pages8
JournalAgents and Actions
Volume38
Issue numberSUPPL. III
Publication statusPublished - Jan 1 1992

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ASJC Scopus subject areas

  • Toxicology
  • Pharmacology (medical)

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