Analysis of the mechanism of the vasodepressor effect of urocortin in anesthetized rats

Aly M. Abdelrahman, Harley T T Syyong, Anindita A G Tjahjadi, Catherine C Y Pang

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7 Citations (Scopus)

Abstract

The aim was to examine if the depressor effect of urocortin involves activation of the nitric oxide (NO)/L-arginine pathway, production of prostanoids or opening of K+-channels. I. v. bolus urocortin (0.1-3 nmol/kg) dose-dependently decreased mean arterial pressure in thiobutabarbital-anesthetized rats. The depressor effect of urocortin was unaffected by pretreatment with NG-nitro-L.-arginine methyl ester (L-NAME, inhibitor of NO synthase, i.v. bolus) or noradrenaline (i.v. infusion), which increased arterial pressure to a similar level as that produced by L-NAME. In addition, methylene blue (inhibitor of soluble guanylyl cyclase, i.v. infusion), indomethacin (cyclooxygenase inhibitor, i.v. bolus), glibenclamide (blocker of ATP-sensitive K+-channels, i.v. bolus) ortetraethylammonium (a non specific K+-channel blocker, i.v. bolus) did not affect the depressor effect of urocortin. In conclusion, the depressor effect of urocortin in anesthetized rats is not mediated via the NO/L.-arginine pathway, activation of soluble guanylyl cyclase, production of prostanoids, opening of TEA sensitive K+-channels nor opening of ATP sensitive K+-channels.

Original languageEnglish
Pages (from-to)175-179
Number of pages5
JournalPharmacology
Volume73
Issue number4
DOIs
Publication statusPublished - 2005

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Keywords

  • Blood pressure
  • Inhibitors of NO synthase
  • K-channels
  • Prostanoids
  • Soluble guanylyl cyclase
  • Urocortin

ASJC Scopus subject areas

  • Pharmacology

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