Possible mechanism of the vasodepressor effect of endokinin a/b in anesthetized rats.

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 NG-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.

journal_name

J Cardiovasc Pharmacol

authors

Abdelrahman AM,Syyong H,Tjahjadi A,Pang CC

doi

10.1097/01.fjc.0000175236.41573.2a

subject

Has Abstract

pub_date

2005-09-01 00:00:00

pages

269-73

issue

3

eissn

0160-2446

issn

1533-4023

pii

00005344-200509000-00005

journal_volume

46

pub_type

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