Possible mechanism of the vasodepressor effect of endokinin A/B in anesthetized rats

Aly Mohamed Abdelrahman, Harley Syyong, Anindita Tjahjadi, Catherine Cheuk Ying Pang

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

We investigated the mechanism of the vasodepressor effect of endokinin A/B. An intravenous (IV) bolus of endokinin A/B (0.05-0.3 nmol/kg) dose-dependently decreased mean arterial pressure in thiobutabarbital-anesthetized rats. The magnitude of the response was unaffected by IV pretreatment with N G-nitro-L-arginine methyl ester (L-NAME, inhibitor of nitric oxide synthase), methylene blue (inhibitor of soluble guanylyl cyclase), indomethacin (cyclooxygenase inhibitor), or tetraethylammonium (TEA, nonspecific K + channel blocker). L-NAME reduced the half-recovery time of the vasodepressor effect of endokinin A/B relative to responses in rats pretreated with either saline or norepinephrine, which caused a similar pressor effect as did L-NAME. Methylene blue, but not TEA or indomethacin, reduced the recovery time of the vasodepressor effect of endokinin A/B. Therefore, the vasodepressor effect of endokinin A/B is mediated via the nitric oxide/L-arginine pathway and activation of soluble guanylyl cyclase but not by production of prostanoids or opening of TEA-sensitive K+ channels.

Original languageEnglish
Pages (from-to)269-273
Number of pages5
JournalJournal of Cardiovascular Pharmacology
Volume46
Issue number3
DOIs
Publication statusPublished - Sep 2005

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Keywords

  • Blood pressure
  • Endokinin A/B
  • Inhibitor of nitric oxide synthase
  • K channel
  • Prostanoids
  • Soluble guanylyl cyclase

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

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