Physiological concentration of 17β-estradiol retards the progression of severe atherosclerosis induced by a high-cholesterol diet plus balloon catheter injury: Role of NO

Toshio Hayashi, Muthuvel Jayachandran, Daigo Sumi, Navin Kumar Thakur, Teiji Esaki, Emiko Muto, Hatsuyo Kano, Yukako Asai, Akihisa Iguchi

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

The molecular mechanisms of the antiatherosclerotic effects of estrogen are not yet known. We evaluated the effects of 17β-estradiol (E2) on high cholesterol diet- (HCD; standard diet and 1% cholesterol) and balloon injury- induced atherosclerosis in female New Zealand White rabbits. The abdominal aortas of 40 oophorectomized (Groups 1 through 5) and 8 nonoophorectomized (Group 6) rabbits were injured by balloon catheter, and the animals were then divided into the following groups and treated for 10 weeks: Group 1, standard diet; Group 2, standard diet plus a moderate dose of E2 (100 μg · kg-1 · d-1); Group 3, HCD; Group 4, HCD plus a moderate dose of E2; Group 5, HCD plus a low dose of E2 (20 μg · kg-1 · d-1); and Group 6, HCD in nonoophorectomized rabbits. After the treatment phase, plasma E2 was increased up to 282.2±45.5 pg/mL in Group 2, 263.0±41.5 pg/mL in Group 4, 87.9±18.8 pg/mL in Group 5, and 45.6±7.3 pg/mL in Group 6. HCD-mediated increases in plasma lipid levels were not changed by E2 treatment, whereas E2 decreased the aortic intimal thickening in Group 2 animals compared with those in Group 1 and reduced atherosclerosis in the thoracic and abdominal aortas of Group 4, 5, and 6 rabbits compared with those in Group 3. E2 restored the impaired abdominal aortic endothelium-dependent relaxation of balloon-injured and HCD-supplemented rabbits, and E2 increased basal nitric oxide (NO) release. The basal NO-releasing effect showed a significant, inverse relation with the severity of atherosclerosis. Plasma E2 concentration also showed a significant, inverse relation with atherosclerotic area. In conclusion, physiological concentrations of E2 can retard the progression of severe atherosclerosis and stabilize atheromas induced by HCD and balloon injury. The retardation may be partially mediated by endothelial NO function in vessels treated with E2.

Original languageEnglish (US)
Pages (from-to)1613-1621
Number of pages9
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume20
Issue number6
StatePublished - Jun 2000
Externally publishedYes

Fingerprint

Estradiol
Atherosclerosis
Nitric Oxide
Catheters
Cholesterol
Diet
Rabbits
Wounds and Injuries
Abdominal Aorta
Tunica Intima
Atherosclerotic Plaques
Thoracic Aorta
Endothelium
Estrogens
Lipids

Keywords

  • Arteriosclerosis
  • Balloon injury
  • Endothelium
  • Estradiol
  • Nitric oxide

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Physiological concentration of 17β-estradiol retards the progression of severe atherosclerosis induced by a high-cholesterol diet plus balloon catheter injury : Role of NO. / Hayashi, Toshio; Jayachandran, Muthuvel; Sumi, Daigo; Thakur, Navin Kumar; Esaki, Teiji; Muto, Emiko; Kano, Hatsuyo; Asai, Yukako; Iguchi, Akihisa.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 20, No. 6, 06.2000, p. 1613-1621.

Research output: Contribution to journalArticle

Hayashi, Toshio ; Jayachandran, Muthuvel ; Sumi, Daigo ; Thakur, Navin Kumar ; Esaki, Teiji ; Muto, Emiko ; Kano, Hatsuyo ; Asai, Yukako ; Iguchi, Akihisa. / Physiological concentration of 17β-estradiol retards the progression of severe atherosclerosis induced by a high-cholesterol diet plus balloon catheter injury : Role of NO. In: Arteriosclerosis, Thrombosis, and Vascular Biology. 2000 ; Vol. 20, No. 6. pp. 1613-1621.
@article{cdf342fada65486ab8efd247b23b7da6,
title = "Physiological concentration of 17β-estradiol retards the progression of severe atherosclerosis induced by a high-cholesterol diet plus balloon catheter injury: Role of NO",
abstract = "The molecular mechanisms of the antiatherosclerotic effects of estrogen are not yet known. We evaluated the effects of 17β-estradiol (E2) on high cholesterol diet- (HCD; standard diet and 1{\%} cholesterol) and balloon injury- induced atherosclerosis in female New Zealand White rabbits. The abdominal aortas of 40 oophorectomized (Groups 1 through 5) and 8 nonoophorectomized (Group 6) rabbits were injured by balloon catheter, and the animals were then divided into the following groups and treated for 10 weeks: Group 1, standard diet; Group 2, standard diet plus a moderate dose of E2 (100 μg · kg-1 · d-1); Group 3, HCD; Group 4, HCD plus a moderate dose of E2; Group 5, HCD plus a low dose of E2 (20 μg · kg-1 · d-1); and Group 6, HCD in nonoophorectomized rabbits. After the treatment phase, plasma E2 was increased up to 282.2±45.5 pg/mL in Group 2, 263.0±41.5 pg/mL in Group 4, 87.9±18.8 pg/mL in Group 5, and 45.6±7.3 pg/mL in Group 6. HCD-mediated increases in plasma lipid levels were not changed by E2 treatment, whereas E2 decreased the aortic intimal thickening in Group 2 animals compared with those in Group 1 and reduced atherosclerosis in the thoracic and abdominal aortas of Group 4, 5, and 6 rabbits compared with those in Group 3. E2 restored the impaired abdominal aortic endothelium-dependent relaxation of balloon-injured and HCD-supplemented rabbits, and E2 increased basal nitric oxide (NO) release. The basal NO-releasing effect showed a significant, inverse relation with the severity of atherosclerosis. Plasma E2 concentration also showed a significant, inverse relation with atherosclerotic area. In conclusion, physiological concentrations of E2 can retard the progression of severe atherosclerosis and stabilize atheromas induced by HCD and balloon injury. The retardation may be partially mediated by endothelial NO function in vessels treated with E2.",
keywords = "Arteriosclerosis, Balloon injury, Endothelium, Estradiol, Nitric oxide",
author = "Toshio Hayashi and Muthuvel Jayachandran and Daigo Sumi and Thakur, {Navin Kumar} and Teiji Esaki and Emiko Muto and Hatsuyo Kano and Yukako Asai and Akihisa Iguchi",
year = "2000",
month = "6",
language = "English (US)",
volume = "20",
pages = "1613--1621",
journal = "Arteriosclerosis, Thrombosis, and Vascular Biology",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Physiological concentration of 17β-estradiol retards the progression of severe atherosclerosis induced by a high-cholesterol diet plus balloon catheter injury

T2 - Role of NO

AU - Hayashi, Toshio

AU - Jayachandran, Muthuvel

AU - Sumi, Daigo

AU - Thakur, Navin Kumar

AU - Esaki, Teiji

AU - Muto, Emiko

AU - Kano, Hatsuyo

AU - Asai, Yukako

AU - Iguchi, Akihisa

PY - 2000/6

Y1 - 2000/6

N2 - The molecular mechanisms of the antiatherosclerotic effects of estrogen are not yet known. We evaluated the effects of 17β-estradiol (E2) on high cholesterol diet- (HCD; standard diet and 1% cholesterol) and balloon injury- induced atherosclerosis in female New Zealand White rabbits. The abdominal aortas of 40 oophorectomized (Groups 1 through 5) and 8 nonoophorectomized (Group 6) rabbits were injured by balloon catheter, and the animals were then divided into the following groups and treated for 10 weeks: Group 1, standard diet; Group 2, standard diet plus a moderate dose of E2 (100 μg · kg-1 · d-1); Group 3, HCD; Group 4, HCD plus a moderate dose of E2; Group 5, HCD plus a low dose of E2 (20 μg · kg-1 · d-1); and Group 6, HCD in nonoophorectomized rabbits. After the treatment phase, plasma E2 was increased up to 282.2±45.5 pg/mL in Group 2, 263.0±41.5 pg/mL in Group 4, 87.9±18.8 pg/mL in Group 5, and 45.6±7.3 pg/mL in Group 6. HCD-mediated increases in plasma lipid levels were not changed by E2 treatment, whereas E2 decreased the aortic intimal thickening in Group 2 animals compared with those in Group 1 and reduced atherosclerosis in the thoracic and abdominal aortas of Group 4, 5, and 6 rabbits compared with those in Group 3. E2 restored the impaired abdominal aortic endothelium-dependent relaxation of balloon-injured and HCD-supplemented rabbits, and E2 increased basal nitric oxide (NO) release. The basal NO-releasing effect showed a significant, inverse relation with the severity of atherosclerosis. Plasma E2 concentration also showed a significant, inverse relation with atherosclerotic area. In conclusion, physiological concentrations of E2 can retard the progression of severe atherosclerosis and stabilize atheromas induced by HCD and balloon injury. The retardation may be partially mediated by endothelial NO function in vessels treated with E2.

AB - The molecular mechanisms of the antiatherosclerotic effects of estrogen are not yet known. We evaluated the effects of 17β-estradiol (E2) on high cholesterol diet- (HCD; standard diet and 1% cholesterol) and balloon injury- induced atherosclerosis in female New Zealand White rabbits. The abdominal aortas of 40 oophorectomized (Groups 1 through 5) and 8 nonoophorectomized (Group 6) rabbits were injured by balloon catheter, and the animals were then divided into the following groups and treated for 10 weeks: Group 1, standard diet; Group 2, standard diet plus a moderate dose of E2 (100 μg · kg-1 · d-1); Group 3, HCD; Group 4, HCD plus a moderate dose of E2; Group 5, HCD plus a low dose of E2 (20 μg · kg-1 · d-1); and Group 6, HCD in nonoophorectomized rabbits. After the treatment phase, plasma E2 was increased up to 282.2±45.5 pg/mL in Group 2, 263.0±41.5 pg/mL in Group 4, 87.9±18.8 pg/mL in Group 5, and 45.6±7.3 pg/mL in Group 6. HCD-mediated increases in plasma lipid levels were not changed by E2 treatment, whereas E2 decreased the aortic intimal thickening in Group 2 animals compared with those in Group 1 and reduced atherosclerosis in the thoracic and abdominal aortas of Group 4, 5, and 6 rabbits compared with those in Group 3. E2 restored the impaired abdominal aortic endothelium-dependent relaxation of balloon-injured and HCD-supplemented rabbits, and E2 increased basal nitric oxide (NO) release. The basal NO-releasing effect showed a significant, inverse relation with the severity of atherosclerosis. Plasma E2 concentration also showed a significant, inverse relation with atherosclerotic area. In conclusion, physiological concentrations of E2 can retard the progression of severe atherosclerosis and stabilize atheromas induced by HCD and balloon injury. The retardation may be partially mediated by endothelial NO function in vessels treated with E2.

KW - Arteriosclerosis

KW - Balloon injury

KW - Endothelium

KW - Estradiol

KW - Nitric oxide

UR - http://www.scopus.com/inward/record.url?scp=0033625348&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033625348&partnerID=8YFLogxK

M3 - Article

C2 - 10845880

AN - SCOPUS:0033625348

VL - 20

SP - 1613

EP - 1621

JO - Arteriosclerosis, Thrombosis, and Vascular Biology

JF - Arteriosclerosis, Thrombosis, and Vascular Biology

SN - 1079-5642

IS - 6

ER -