Extracellular and intracellular arachidonic acid-induced contractions in rat aorta

CM Filipeanu, E Brailoiu, G Petrescu, SA Nelemans*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

6 Citations (Scopus)

Abstract

Arachidonic acid induced contractions of de-endothelized rat aortic rings. A more potent effect was obtained after intracellular administration of arachidonic acid using liposomes. Contractions induced by extracellular arachidonic acid were inhibited similarly to phenylephrine-induced contractions by the L-type Ca2+ channel blocker, methoxyverapamil (D600), and the calmodulin inhibitor, calmidazolium. In contrast, contractions induced by arachidonic acid-filled liposomes were not affected by these compounds. Indomethacin did not affect the contractions induced by either extra- or intracellular arachidonic acid, whereas nordihydroguaiaretic acid relaxed contractions induced by extracellular arachidonic acid but not those induced by arachidonic acid-filled liposomes. Apart from a relaxing effect on contractions induced by extracellular arachidonic acid or by phenylephrine, protein kinase C inhibition with 1-(5-isoquinolinesulphonyl-2-methylpiperazine (H7)) had an even more prominent relaxing effect on contractions induced by arachidonic acid-filled liposomes. Therefore, arachidonic acid exerts a contractile effect on rat aorta, and this effect is regulated differently depending on the site of application. (C) 1998 Elsevier Science B.V. All rights reserved.

Original languageEnglish
Pages (from-to)67-73
Number of pages7
JournalEuropean Journal of Pharmacology
Volume349
Issue number1
Publication statusPublished - 15-May-1998

Keywords

  • arachidonic acid
  • smooth muscle
  • aorta
  • contraction
  • liposome
  • PROTEIN-KINASE-C
  • SMOOTH-MUSCLE
  • FATTY-ACIDS
  • CELLS
  • CALCIUM
  • MOBILIZATION
  • STIMULATION
  • HOMEOSTASIS
  • ACTIVATION
  • LIPOSOMES

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