1999PubMedRequires access

Valsartan inhibits angiotensin II-stimulated proliferation of smooth muscle cells from human coronary artery.

Mueck Ao, Harald Seeger, Lippert Th

Open publisher page 18 citations

Abstract

OBJECTIVES: Angiotensin II is involved in the pathogenesis of atherosclerosis by inducing hyperproliferation of vascular smooth muscle cells. Little is known whether the sartans can inhibit the angiotensin-stimulated proliferation of smooth muscle cells. METHOD: The effect of valsartan on the angiotensin II-stimulated proliferation of smooth muscle cells from human coronary artery was investigated. RESULTS: Angiotensin II significantly increased cell proliferation by about 30% at a concentration of 10(-6) M without significant changes at the lower concentrations 10(-7) and 10(-8) M. Valsartan at the dosages 10(-8) to 10(-6) M had no effect on serum-stimulated proliferation. Valsartan at the dosages 10(-6) and 10(-7) M inhibited the cell proliferation induced by 10(-6) M angiotensin. CONCLUSION: Valsartan may prevent atherosclerosis by inhibiting angiotensin-induced vascular smooth muscle cell proliferation.

About this research paper

What this paper is about

OBJECTIVES: Angiotensin II is involved in the pathogenesis of atherosclerosis by inducing hyperproliferation of vascular smooth muscle cells. Little is known whether the sartans can inhibit the angiotensin-stimulated proliferation of smooth muscle cells. METHOD: The effect of valsartan on the angiotensin II-stimulated proliferation of smooth muscle cells from human coronary artery was investigated. RESULTS: Angiotensin II significantly increased cell proliferation by about 30% at a concentration of 10(-6) M without significant changes at the lower concentrations 10(-7) and 10(-8) M. Valsartan at the dosages 10(-8) to 10(-6) M had no effect on serum-stimulated proliferation. Valsartan at the dosages 10(-6) and 10(-7) M inhibited the cell proliferation induced by 10(-6) M angiotensin. CONCLUSION: Valsartan may prevent atherosclerosis by inhibiting angiotensin-induced vascular smooth muscle cell proliferation.

Why it matters

OpenAlex reports 18 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

OBJECTIVES: Angiotensin II is involved in the pathogenesis of atherosclerosis by inducing hyperproliferation of vascular smooth muscle cells. Little is known whether the sartans can inhibit the angiotensin-stimulated proliferation of smooth muscle cells. METHOD: The effect of valsartan on the angiotensin II-stimulated proliferation of smooth muscle cells from human coronary artery was investigated. RESULTS: Angiotensin II significantly increased cell proliferation by about 30% at a concentration of 10(-6) M without significant changes at the lower concentrations 10(-7) and 10(-8) M. Valsartan at the dosages 10(-8) to 10(-6) M had no effect on serum-stimulated proliferation. Valsartan at the dosages 10(-6) and 10(-7) M inhibited the cell proliferation induced by 10(-6) M angiotensin. CONCLUSION: Valsartan may prevent atherosclerosis by inhibiting angiotensin-induced vascular smooth muscle cell proliferation.

Key concepts: Valsartan, Angiotensin II, Vascular smooth muscle, Cell growth, Internal medicine, Endocrinology, Renin–angiotensin system, Angiotensin receptor

Related papers

Back to paper searchBrowse research topicsOriginal source
Valsartan inhibits angiotensin II-stimulated proliferation of smooth muscle cells from human coronary artery. — Research Paper | ScholarLens