Chronic fluvastatin treatment alters vascular contraction by inhibiting the Rho/Rho-kinase pathway

Yasuo Kansui, Koji Fujii, Kenichi Goto, Hideyuki Oniki, Mitsuo Iida

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

1. In the present study, we investigated the effects of chronic treatment of stroke-prone spontaneously hypertensive rats (SHRSP) with the statin fluvastatin on vascular Rho/Rho-kinase pathway mediated contraction, which has been shown to be upregulated in hypertension. 2. Contribution of the Rho/Rho-kinase pathway to noradrenaline-induced contraction of arteries from SHRSP was assessed by the inhibitory effect of Y-27632, a Rho/Rho-kinase inhibitor. Stroke-prone spontaneously hypertensive rats were treated with fluvastatin (10 mg/kg per day) for 1 month. 3. Treatment with fluvastatin tended to attenuate the contraction to noradrenaline and significantly decreased the Y-27632-sensitive component of the contraction in controls compared with fluvastatin-treated rats. 4. RhoA, as assessed by western blotting, was also reduced by fluvastatin treatment. 5. These findings suggest that chronic treatment with fluvastatin reduces the contractile response associated with Rho/Rho-kinase in arteries of hypertensive rats.

Original languageEnglish
Pages (from-to)673-678
Number of pages6
JournalClinical and Experimental Pharmacology and Physiology
Volume33
Issue number8
DOIs
Publication statusPublished - Aug 1 2006

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fluvastatin
rho-Associated Kinases
Blood Vessels
Inbred SHR Rats
Norepinephrine
Arteries
Stroke
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Western Blotting

All Science Journal Classification (ASJC) codes

  • Physiology
  • Pharmacology
  • Physiology (medical)

Cite this

Chronic fluvastatin treatment alters vascular contraction by inhibiting the Rho/Rho-kinase pathway. / Kansui, Yasuo; Fujii, Koji; Goto, Kenichi; Oniki, Hideyuki; Iida, Mitsuo.

In: Clinical and Experimental Pharmacology and Physiology, Vol. 33, No. 8, 01.08.2006, p. 673-678.

Research output: Contribution to journalArticle

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