Contribution of arachidonic acid metabolites derived via cytochrome P4504A to angiotensin II-induced neointimal growth

Fariborz A. Yaghini, Chunxiang Zhang, Jean Hugues Parmentier, Anne M. Estes, Nauzanene Jafari, Susan A. Schaefer, Kafait Malik

Research output: Contribution to journalArticle

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Abstract

Angiotensin II and the arachidonic acid metabolite derived via cytochrome P450 20-hydroxyeicostetraenoic acid promote vasoconstriction and vascular smooth muscle cell (VSMC) proliferation. This study was conducted to determine if 20-hydroxyeicostetraenoic acid contributes to angiotensin II-induced neointimal formation in balloon-injured rat carotid artery. In anesthetized rats, the drugs were infused into the clamped segment of the injured right common carotid artery for 60 minutes. The drug solution and catheter were withdrawn, the common carotid artery was ligated, and blood flow was restored. Exposure of the injured artery to angiotensin II (200 nmol/L) or arachidonic acid (10 μmol/L) increased neointimal thickening at day 14 (intima/media ratio 0.71±0.14 with vehicle versus 1.65±0.10 with angiotensin II or 1.31±0.13 with arachidonic acid; P<0.05). Cytochrome P450 4A1 antisense, but not scrambled, oligodeoxynucleotide (100 nmol/L) reduced angiotensin II-induced or arachidonic acid-induced neointimal thickening (intima/media ratio 0.90±0.07 for angiotensin II and 0.95±0.06 for arachidonic acid). 20-hydroxyeicostetraenoic acid (0.5 μmol/L) also increased neointimal thickening of injured artery (intima/media ratio 1.1.5±0.03); this was not altered by cytochrome P450 4A1 antisense oligodeoxynucleotide. Angiotensin II. arachidonic acid, and 20-hydroxyeicostetraenoic acid also induced the expression of cytochrome P450 4A and increased the number of CD45-positive cells; the latter effect of angiotensin II and arachidonic acid, but not 20-hydroxyeicostetraenoic acid, was diminished by cytochrome P450 4A1 antisense oligodeoxynucleotide. These data suggest that arachidonic acid metabolites derived via cytochrome P450 4A, most likely 20-hydroxyeicostetraenoic acid, mediate angiotensin II-induced neointimal thickening in injured rat carotid artery.

Original languageEnglish (US)
Pages (from-to)1182-1187
Number of pages6
JournalHypertension
Volume45
Issue number6
DOIs
StatePublished - Jun 1 2005

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Cytochromes
Arachidonic Acid
Angiotensin II
Cytochrome P-450 Enzyme System
Growth
Acids
Oligodeoxyribonucleotides
Common Carotid Artery
Carotid Arteries
Arteries
Vasoconstriction
Vascular Smooth Muscle
Pharmaceutical Preparations
Smooth Muscle Myocytes
Catheters
Cell Proliferation

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Contribution of arachidonic acid metabolites derived via cytochrome P4504A to angiotensin II-induced neointimal growth. / Yaghini, Fariborz A.; Zhang, Chunxiang; Parmentier, Jean Hugues; Estes, Anne M.; Jafari, Nauzanene; Schaefer, Susan A.; Malik, Kafait.

In: Hypertension, Vol. 45, No. 6, 01.06.2005, p. 1182-1187.

Research output: Contribution to journalArticle

Yaghini, Fariborz A. ; Zhang, Chunxiang ; Parmentier, Jean Hugues ; Estes, Anne M. ; Jafari, Nauzanene ; Schaefer, Susan A. ; Malik, Kafait. / Contribution of arachidonic acid metabolites derived via cytochrome P4504A to angiotensin II-induced neointimal growth. In: Hypertension. 2005 ; Vol. 45, No. 6. pp. 1182-1187.
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abstract = "Angiotensin II and the arachidonic acid metabolite derived via cytochrome P450 20-hydroxyeicostetraenoic acid promote vasoconstriction and vascular smooth muscle cell (VSMC) proliferation. This study was conducted to determine if 20-hydroxyeicostetraenoic acid contributes to angiotensin II-induced neointimal formation in balloon-injured rat carotid artery. In anesthetized rats, the drugs were infused into the clamped segment of the injured right common carotid artery for 60 minutes. The drug solution and catheter were withdrawn, the common carotid artery was ligated, and blood flow was restored. Exposure of the injured artery to angiotensin II (200 nmol/L) or arachidonic acid (10 μmol/L) increased neointimal thickening at day 14 (intima/media ratio 0.71±0.14 with vehicle versus 1.65±0.10 with angiotensin II or 1.31±0.13 with arachidonic acid; P<0.05). Cytochrome P450 4A1 antisense, but not scrambled, oligodeoxynucleotide (100 nmol/L) reduced angiotensin II-induced or arachidonic acid-induced neointimal thickening (intima/media ratio 0.90±0.07 for angiotensin II and 0.95±0.06 for arachidonic acid). 20-hydroxyeicostetraenoic acid (0.5 μmol/L) also increased neointimal thickening of injured artery (intima/media ratio 1.1.5±0.03); this was not altered by cytochrome P450 4A1 antisense oligodeoxynucleotide. Angiotensin II. arachidonic acid, and 20-hydroxyeicostetraenoic acid also induced the expression of cytochrome P450 4A and increased the number of CD45-positive cells; the latter effect of angiotensin II and arachidonic acid, but not 20-hydroxyeicostetraenoic acid, was diminished by cytochrome P450 4A1 antisense oligodeoxynucleotide. These data suggest that arachidonic acid metabolites derived via cytochrome P450 4A, most likely 20-hydroxyeicostetraenoic acid, mediate angiotensin II-induced neointimal thickening in injured rat carotid artery.",
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