Insulin-like growth factor inhibits vascular contraction to 5- hydroxytryptamine

Involvement of tyrosine phosphatase

Alessandra Melis, Stephanie W. Watts, Jennifer Florian, Susan Klarr, R Clinton Webb

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

This study tests the hypothesis that insulin-like growth factor 1 (IGF- 1)-induced vasodilation is due to the stimulation of tyrosine phosphatase. Rat aortic segments (endothelium intact) were placed in muscle baths for force measurement. Segments were contracted to serotonin [5-hydroxytyptamine (5-HT), 10-7-10-5 M] before and after incubation with IGF-1 (10-100 nM; 90 min). IGF-1 caused a 20% inhibition of 5-HT-induced contractions. This inhibition was reversed by the tyrosine phosphatase inhibitors sodium orthovanadate and molybdate. Orthovanadate did not alter inhibitory properties of the calcium channel antagonist verapamil, suggesting that the phosphatase inhibitors were relatively specific. IGF-1-induced inhibition was not altered by blockade of nitric oxide synthase. Western blot analysis confirmed that the 5-HT-induced stimulation of tyrosine phosphorylation of the 42-kDa extracellular signal-regulated mitogen-activated protein kinase protein was reduced by IGF-1 (52% inhibition), an inhibition that was attenuated by orthovanadate. These data are consistent with the hypothesis that the vasodilator activity of IGF-1 is mediated by the activation of a tyrosine phosphatase. (C) 2000 Elsevier Science Inc.

Original languageEnglish (US)
Pages (from-to)137-145
Number of pages9
JournalGeneral Pharmacology
Volume34
Issue number2
DOIs
StatePublished - Feb 1 2000
Externally publishedYes

Fingerprint

Somatomedins
Insulin-Like Growth Factor I
Phosphoric Monoester Hydrolases
Blood Vessels
Tyrosine
Serotonin
Vanadates
Calcium Channel Blockers
Verapamil
Mitogen-Activated Protein Kinases
Vasodilator Agents
Baths
Vasodilation
Nitric Oxide Synthase
Endothelium
Western Blotting
Phosphorylation
Muscles
Proteins

Keywords

  • Insulin-like growth factor
  • Orthovanadate
  • Rat aorta
  • Tyrosine phosphatase

ASJC Scopus subject areas

  • Pharmacology

Cite this

Insulin-like growth factor inhibits vascular contraction to 5- hydroxytryptamine : Involvement of tyrosine phosphatase. / Melis, Alessandra; Watts, Stephanie W.; Florian, Jennifer; Klarr, Susan; Webb, R Clinton.

In: General Pharmacology, Vol. 34, No. 2, 01.02.2000, p. 137-145.

Research output: Contribution to journalArticle

Melis, Alessandra ; Watts, Stephanie W. ; Florian, Jennifer ; Klarr, Susan ; Webb, R Clinton. / Insulin-like growth factor inhibits vascular contraction to 5- hydroxytryptamine : Involvement of tyrosine phosphatase. In: General Pharmacology. 2000 ; Vol. 34, No. 2. pp. 137-145.
@article{19ce441f0def483b91ae50296fb570d3,
title = "Insulin-like growth factor inhibits vascular contraction to 5- hydroxytryptamine: Involvement of tyrosine phosphatase",
abstract = "This study tests the hypothesis that insulin-like growth factor 1 (IGF- 1)-induced vasodilation is due to the stimulation of tyrosine phosphatase. Rat aortic segments (endothelium intact) were placed in muscle baths for force measurement. Segments were contracted to serotonin [5-hydroxytyptamine (5-HT), 10-7-10-5 M] before and after incubation with IGF-1 (10-100 nM; 90 min). IGF-1 caused a 20{\%} inhibition of 5-HT-induced contractions. This inhibition was reversed by the tyrosine phosphatase inhibitors sodium orthovanadate and molybdate. Orthovanadate did not alter inhibitory properties of the calcium channel antagonist verapamil, suggesting that the phosphatase inhibitors were relatively specific. IGF-1-induced inhibition was not altered by blockade of nitric oxide synthase. Western blot analysis confirmed that the 5-HT-induced stimulation of tyrosine phosphorylation of the 42-kDa extracellular signal-regulated mitogen-activated protein kinase protein was reduced by IGF-1 (52{\%} inhibition), an inhibition that was attenuated by orthovanadate. These data are consistent with the hypothesis that the vasodilator activity of IGF-1 is mediated by the activation of a tyrosine phosphatase. (C) 2000 Elsevier Science Inc.",
keywords = "Insulin-like growth factor, Orthovanadate, Rat aorta, Tyrosine phosphatase",
author = "Alessandra Melis and Watts, {Stephanie W.} and Jennifer Florian and Susan Klarr and Webb, {R Clinton}",
year = "2000",
month = "2",
day = "1",
doi = "10.1016/S0306-3623(00)00055-0",
language = "English (US)",
volume = "34",
pages = "137--145",
journal = "Vascular Pharmacology",
issn = "1537-1891",
publisher = "Elsevier Inc.",
number = "2",

}

TY - JOUR

T1 - Insulin-like growth factor inhibits vascular contraction to 5- hydroxytryptamine

T2 - Involvement of tyrosine phosphatase

AU - Melis, Alessandra

AU - Watts, Stephanie W.

AU - Florian, Jennifer

AU - Klarr, Susan

AU - Webb, R Clinton

PY - 2000/2/1

Y1 - 2000/2/1

N2 - This study tests the hypothesis that insulin-like growth factor 1 (IGF- 1)-induced vasodilation is due to the stimulation of tyrosine phosphatase. Rat aortic segments (endothelium intact) were placed in muscle baths for force measurement. Segments were contracted to serotonin [5-hydroxytyptamine (5-HT), 10-7-10-5 M] before and after incubation with IGF-1 (10-100 nM; 90 min). IGF-1 caused a 20% inhibition of 5-HT-induced contractions. This inhibition was reversed by the tyrosine phosphatase inhibitors sodium orthovanadate and molybdate. Orthovanadate did not alter inhibitory properties of the calcium channel antagonist verapamil, suggesting that the phosphatase inhibitors were relatively specific. IGF-1-induced inhibition was not altered by blockade of nitric oxide synthase. Western blot analysis confirmed that the 5-HT-induced stimulation of tyrosine phosphorylation of the 42-kDa extracellular signal-regulated mitogen-activated protein kinase protein was reduced by IGF-1 (52% inhibition), an inhibition that was attenuated by orthovanadate. These data are consistent with the hypothesis that the vasodilator activity of IGF-1 is mediated by the activation of a tyrosine phosphatase. (C) 2000 Elsevier Science Inc.

AB - This study tests the hypothesis that insulin-like growth factor 1 (IGF- 1)-induced vasodilation is due to the stimulation of tyrosine phosphatase. Rat aortic segments (endothelium intact) were placed in muscle baths for force measurement. Segments were contracted to serotonin [5-hydroxytyptamine (5-HT), 10-7-10-5 M] before and after incubation with IGF-1 (10-100 nM; 90 min). IGF-1 caused a 20% inhibition of 5-HT-induced contractions. This inhibition was reversed by the tyrosine phosphatase inhibitors sodium orthovanadate and molybdate. Orthovanadate did not alter inhibitory properties of the calcium channel antagonist verapamil, suggesting that the phosphatase inhibitors were relatively specific. IGF-1-induced inhibition was not altered by blockade of nitric oxide synthase. Western blot analysis confirmed that the 5-HT-induced stimulation of tyrosine phosphorylation of the 42-kDa extracellular signal-regulated mitogen-activated protein kinase protein was reduced by IGF-1 (52% inhibition), an inhibition that was attenuated by orthovanadate. These data are consistent with the hypothesis that the vasodilator activity of IGF-1 is mediated by the activation of a tyrosine phosphatase. (C) 2000 Elsevier Science Inc.

KW - Insulin-like growth factor

KW - Orthovanadate

KW - Rat aorta

KW - Tyrosine phosphatase

UR - http://www.scopus.com/inward/record.url?scp=0033839142&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033839142&partnerID=8YFLogxK

U2 - 10.1016/S0306-3623(00)00055-0

DO - 10.1016/S0306-3623(00)00055-0

M3 - Article

VL - 34

SP - 137

EP - 145

JO - Vascular Pharmacology

JF - Vascular Pharmacology

SN - 1537-1891

IS - 2

ER -