Details
| Originalsprache | Englisch |
|---|---|
| Seiten (von - bis) | 247-249 |
| Seitenumfang | 3 |
| Fachzeitschrift | European journal of pharmacology |
| Jahrgang | 512 |
| Ausgabenummer | 2-3 |
| Frühes Online-Datum | 31 März 2005 |
| Publikationsstatus | Veröffentlicht - 11 Apr. 2005 |
| Extern publiziert | Ja |
Abstract
Chronic inhibition of Rho-kinase has been recently implicated in retardation of atherogenesis induced by high-fat diet in low-density lipoprotein receptor deficient (LDLR-/-) mice. However, it remains to be examined whether long-term Rho-kinase inhibition will reduce vascular dysfunction in this model. LDLR-/- mice on a high-fat diet were treated either with saline (LDLR-/-) or with the Rho-kinase inhibitor Fasudil (HA1077, 5-Isoquinolinesulfonyl homopiperazine, 100 mg/kg/day by gavage, LDLR-/- + Fasudil) for 10 weeks. Fasudil-treatment normalized endothelial function (measured by means of endothelium-dependent vasorelaxation) in LDLR-/- + Fasudil, to the level of controls (C57BL/6J). No tolerance toward Rho-kinase inhibition has been detected in Fasudil-treated animals. We conclude that long-term Rho-kinase inhibition normalizes endothelial function without development of tolerance.
ASJC Scopus Sachgebiete
- Pharmakologie, Toxikologie und Pharmazie (insg.)
- Pharmakologie
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in: European journal of pharmacology, Jahrgang 512, Nr. 2-3, 11.04.2005, S. 247-249.
Publikation: Beitrag in Fachzeitschrift › Artikel › Forschung › Peer-Review
}
TY - JOUR
T1 - Long term Rho-kinase inhibition ameliorates endothelial dysfunction in LDL-receptor deficient mice
AU - Steioff, Kerstin
AU - Rütten, Hartmut
AU - Busch, Andreas E.
AU - Plettenburg, Oliver
AU - Ivashchenko, Yuri
AU - Löhn, Matthias
N1 - Funding Information: This work have been supported by INTAS grant Nos. 00-807, 01-2212 and Programmes of the Russian Academy of Sciences “Low Dimensional Quantum Structures”, “Integration”, RFBR (Project No. 02-03-33218). S.V.D. acknowledges financial support from Venture Business Laboratory of Kobe University and Russian Science Support Foundation.
PY - 2005/4/11
Y1 - 2005/4/11
N2 - Chronic inhibition of Rho-kinase has been recently implicated in retardation of atherogenesis induced by high-fat diet in low-density lipoprotein receptor deficient (LDLR-/-) mice. However, it remains to be examined whether long-term Rho-kinase inhibition will reduce vascular dysfunction in this model. LDLR-/- mice on a high-fat diet were treated either with saline (LDLR-/-) or with the Rho-kinase inhibitor Fasudil (HA1077, 5-Isoquinolinesulfonyl homopiperazine, 100 mg/kg/day by gavage, LDLR-/- + Fasudil) for 10 weeks. Fasudil-treatment normalized endothelial function (measured by means of endothelium-dependent vasorelaxation) in LDLR-/- + Fasudil, to the level of controls (C57BL/6J). No tolerance toward Rho-kinase inhibition has been detected in Fasudil-treated animals. We conclude that long-term Rho-kinase inhibition normalizes endothelial function without development of tolerance.
AB - Chronic inhibition of Rho-kinase has been recently implicated in retardation of atherogenesis induced by high-fat diet in low-density lipoprotein receptor deficient (LDLR-/-) mice. However, it remains to be examined whether long-term Rho-kinase inhibition will reduce vascular dysfunction in this model. LDLR-/- mice on a high-fat diet were treated either with saline (LDLR-/-) or with the Rho-kinase inhibitor Fasudil (HA1077, 5-Isoquinolinesulfonyl homopiperazine, 100 mg/kg/day by gavage, LDLR-/- + Fasudil) for 10 weeks. Fasudil-treatment normalized endothelial function (measured by means of endothelium-dependent vasorelaxation) in LDLR-/- + Fasudil, to the level of controls (C57BL/6J). No tolerance toward Rho-kinase inhibition has been detected in Fasudil-treated animals. We conclude that long-term Rho-kinase inhibition normalizes endothelial function without development of tolerance.
KW - Endothelial dysfunction
KW - Hypercholesterolemia
KW - Rho-kinase
UR - http://www.scopus.com/inward/record.url?scp=17444374941&partnerID=8YFLogxK
U2 - 10.1016/j.ejphar.2005.03.001
DO - 10.1016/j.ejphar.2005.03.001
M3 - Article
C2 - 15840411
AN - SCOPUS:17444374941
VL - 512
SP - 247
EP - 249
JO - European journal of pharmacology
JF - European journal of pharmacology
SN - 0014-2999
IS - 2-3
ER -