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

Fingerprint

NG-Nitroarginine Methyl Ester
Methylene Blue
Indomethacin
Tetraethylammonium
Cyclooxygenase Inhibitors
Nitric Oxide Synthase
Prostaglandins
Arginine
Norepinephrine
Arterial Pressure
Nitric Oxide
Soluble Guanylyl Cyclase

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

Cite this

Possible mechanism of the vasodepressor effect of endokinin A/B in anesthetized rats. / Abdelrahman, Aly Mohamed; Syyong, Harley; Tjahjadi, Anindita; Pang, Catherine Cheuk Ying.

In: Journal of Cardiovascular Pharmacology, Vol. 46, No. 3, 09.2005, p. 269-273.

Research output: Contribution to journalArticle

Abdelrahman, Aly Mohamed ; Syyong, Harley ; Tjahjadi, Anindita ; Pang, Catherine Cheuk Ying. / Possible mechanism of the vasodepressor effect of endokinin A/B in anesthetized rats. In: Journal of Cardiovascular Pharmacology. 2005 ; Vol. 46, No. 3. pp. 269-273.
@article{abd027ebbc384e378787f1eabdb7fa3e,
title = "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 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.",
keywords = "Blood pressure, Endokinin A/B, Inhibitor of nitric oxide synthase, K channel, Prostanoids, Soluble guanylyl cyclase",
author = "Abdelrahman, {Aly Mohamed} and Harley Syyong and Anindita Tjahjadi and Pang, {Catherine Cheuk Ying}",
year = "2005",
month = "9",
doi = "10.1097/01.fjc.0000175236.41573.2a",
language = "English",
volume = "46",
pages = "269--273",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Possible mechanism of the vasodepressor effect of endokinin A/B in anesthetized rats

AU - Abdelrahman, Aly Mohamed

AU - Syyong, Harley

AU - Tjahjadi, Anindita

AU - Pang, Catherine Cheuk Ying

PY - 2005/9

Y1 - 2005/9

N2 - 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.

AB - 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.

KW - Blood pressure

KW - Endokinin A/B

KW - Inhibitor of nitric oxide synthase

KW - K channel

KW - Prostanoids

KW - Soluble guanylyl cyclase

UR - http://www.scopus.com/inward/record.url?scp=24344440223&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=24344440223&partnerID=8YFLogxK

U2 - 10.1097/01.fjc.0000175236.41573.2a

DO - 10.1097/01.fjc.0000175236.41573.2a

M3 - Article

C2 - 16116330

AN - SCOPUS:24344440223

VL - 46

SP - 269

EP - 273

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 3

ER -