Melatonin counteracts potentiation by homocysteine of KCl-induced vasoconstriction in human umbilical artery

Relation to calcium influx

Y. Okatani, A. Wakatsuki, Russel J Reiter

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Homocysteinemia is a major and independent risk factor for vascular disease. Oxidative stress is a possible mechanism for homocysteine (HCY)-induced vascular disease. Herein, we evaluated the antioxidant property of melatonin (MLT) in relation to the vasoconstrictive effect of HCY on the human umbilical artery. Helical umbilical arterial strips without endothelium were obtained at elective Cesarean delivery near term. Changes in potassium chloride (KCl)-induced vasoconstriction were measured. Arterial strips were treated with HCY (10 or 100 μM) plus FeSO4 (10 μM) alone or pretreated with a hydroxyl radical (·OH) scavenger, mannitol (20 mM), or MLT (1 or 10 μM). The effect of HCY on the response of arterial strips to external calcium (Ca2+) in the presence of KCl (20 mM) was determined. HCY plus FeSO4 potentiated KCl-induced vasoconstriction in a concentration-dependent manner; pretreatment with mannitol significantly reduced this vasospastic effect. HCY (100 μM) significantly augmented the contractile response to external Ca2+. MLT (10 μM) significantly suppressed the contractile response to external Ca2+. These results suggest that HCY potentiates KCl-induced umbilical artery vasoconstriction, in part by increasing Ca2+ influx in vascular smooth muscle cells via activation of Ca2+ channels. MLT significantly suppressed the vasoconstrictive effect of HCY, probably by scavenging ·OH arising from HCY autooxidation.

Original languageEnglish (US)
Pages (from-to)940-944
Number of pages5
JournalBiochemical and Biophysical Research Communications
Volume280
Issue number3
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Umbilical Arteries
Homocysteine
Melatonin
Vasoconstriction
Calcium
Mannitol
Vascular Diseases
Umbilicus
Oxidative stress
Potassium Chloride
Scavenging
Vascular Smooth Muscle
Hydroxyl Radical
Smooth Muscle Myocytes
Endothelium
Muscle
Oxidative Stress
Antioxidants
Chemical activation
Cells

Keywords

  • Calcium
  • Homocysteine
  • Melatonin
  • Umbilical artery
  • Vasospasm

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

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title = "Melatonin counteracts potentiation by homocysteine of KCl-induced vasoconstriction in human umbilical artery: Relation to calcium influx",
abstract = "Homocysteinemia is a major and independent risk factor for vascular disease. Oxidative stress is a possible mechanism for homocysteine (HCY)-induced vascular disease. Herein, we evaluated the antioxidant property of melatonin (MLT) in relation to the vasoconstrictive effect of HCY on the human umbilical artery. Helical umbilical arterial strips without endothelium were obtained at elective Cesarean delivery near term. Changes in potassium chloride (KCl)-induced vasoconstriction were measured. Arterial strips were treated with HCY (10 or 100 μM) plus FeSO4 (10 μM) alone or pretreated with a hydroxyl radical (·OH) scavenger, mannitol (20 mM), or MLT (1 or 10 μM). The effect of HCY on the response of arterial strips to external calcium (Ca2+) in the presence of KCl (20 mM) was determined. HCY plus FeSO4 potentiated KCl-induced vasoconstriction in a concentration-dependent manner; pretreatment with mannitol significantly reduced this vasospastic effect. HCY (100 μM) significantly augmented the contractile response to external Ca2+. MLT (10 μM) significantly suppressed the contractile response to external Ca2+. These results suggest that HCY potentiates KCl-induced umbilical artery vasoconstriction, in part by increasing Ca2+ influx in vascular smooth muscle cells via activation of Ca2+ channels. MLT significantly suppressed the vasoconstrictive effect of HCY, probably by scavenging ·OH arising from HCY autooxidation.",
keywords = "Calcium, Homocysteine, Melatonin, Umbilical artery, Vasospasm",
author = "Y. Okatani and A. Wakatsuki and Reiter, {Russel J}",
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TY - JOUR

T1 - Melatonin counteracts potentiation by homocysteine of KCl-induced vasoconstriction in human umbilical artery

T2 - Relation to calcium influx

AU - Okatani, Y.

AU - Wakatsuki, A.

AU - Reiter, Russel J

PY - 2001

Y1 - 2001

N2 - Homocysteinemia is a major and independent risk factor for vascular disease. Oxidative stress is a possible mechanism for homocysteine (HCY)-induced vascular disease. Herein, we evaluated the antioxidant property of melatonin (MLT) in relation to the vasoconstrictive effect of HCY on the human umbilical artery. Helical umbilical arterial strips without endothelium were obtained at elective Cesarean delivery near term. Changes in potassium chloride (KCl)-induced vasoconstriction were measured. Arterial strips were treated with HCY (10 or 100 μM) plus FeSO4 (10 μM) alone or pretreated with a hydroxyl radical (·OH) scavenger, mannitol (20 mM), or MLT (1 or 10 μM). The effect of HCY on the response of arterial strips to external calcium (Ca2+) in the presence of KCl (20 mM) was determined. HCY plus FeSO4 potentiated KCl-induced vasoconstriction in a concentration-dependent manner; pretreatment with mannitol significantly reduced this vasospastic effect. HCY (100 μM) significantly augmented the contractile response to external Ca2+. MLT (10 μM) significantly suppressed the contractile response to external Ca2+. These results suggest that HCY potentiates KCl-induced umbilical artery vasoconstriction, in part by increasing Ca2+ influx in vascular smooth muscle cells via activation of Ca2+ channels. MLT significantly suppressed the vasoconstrictive effect of HCY, probably by scavenging ·OH arising from HCY autooxidation.

AB - Homocysteinemia is a major and independent risk factor for vascular disease. Oxidative stress is a possible mechanism for homocysteine (HCY)-induced vascular disease. Herein, we evaluated the antioxidant property of melatonin (MLT) in relation to the vasoconstrictive effect of HCY on the human umbilical artery. Helical umbilical arterial strips without endothelium were obtained at elective Cesarean delivery near term. Changes in potassium chloride (KCl)-induced vasoconstriction were measured. Arterial strips were treated with HCY (10 or 100 μM) plus FeSO4 (10 μM) alone or pretreated with a hydroxyl radical (·OH) scavenger, mannitol (20 mM), or MLT (1 or 10 μM). The effect of HCY on the response of arterial strips to external calcium (Ca2+) in the presence of KCl (20 mM) was determined. HCY plus FeSO4 potentiated KCl-induced vasoconstriction in a concentration-dependent manner; pretreatment with mannitol significantly reduced this vasospastic effect. HCY (100 μM) significantly augmented the contractile response to external Ca2+. MLT (10 μM) significantly suppressed the contractile response to external Ca2+. These results suggest that HCY potentiates KCl-induced umbilical artery vasoconstriction, in part by increasing Ca2+ influx in vascular smooth muscle cells via activation of Ca2+ channels. MLT significantly suppressed the vasoconstrictive effect of HCY, probably by scavenging ·OH arising from HCY autooxidation.

KW - Calcium

KW - Homocysteine

KW - Melatonin

KW - Umbilical artery

KW - Vasospasm

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