Renin-Angiotensin System in Cultured Human Arterial Smooth Muscle Cells

Larrue, J; Demond-Henri, J.; Daret, Danièle

doi:10.1097/00005344-198900000-00010

Cited by 7 publications

(2 citation statements)

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“…[3][4][5][6][7] In vivo, angiotensin II administration increases the hyperplastic response to experimental vessel damage 8 and, after arterial damage, ACE is increased in the neointima with a distribution suggesting that it is associated with VSMC. 9 There is evidence that ACE is actually produced by VSMC in that the enzyme activity [10][11][12][13][14] and messenger RNA (mRNA) for ACE [12][13][14][15] have been found in VSMC. Only one of these studies sought the mRNA in human VSMC.…”

Section: Introductionmentioning

confidence: 99%

ACE inhibition and fibroblast growth factor in cultured human vascular smooth muscle

1999

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Abstract:The effects of the angiotensin converting enzyme (ACE) inhibitor, enalaprilat, and basic fibroblast growth factor (bFGF) on DNA synthesis and expression of ACE mRNA were examined in human vascular smooth muscle cells cultured from saphenous vein and internal mammary artery.DNA synthesis was estimated using 3 H-thymidine uptake, and ACE mRNA was estimated by rt-PCR. Enalaprilat (0.125 g/ml, 48 h) decreased 3 H-thymidine uptake to 66 ± 12% (SE) of the control without enalaprilat (p Ͻ 0.05). Basic FGF (10 ng/ml, 24 h) increased uptake by 41 ± 12% (p Ͻ 0.05) while enalaprilat pretreatment (24 h) decreased uptake to 56 ± 12% of this augmented value (p Ͻ 0.025). Basic FGF increased ACE mRNA, a process that was time dependent with an approximately 50% increase after 24 h exposure. Pre-exposure to enalaprilat (24 h) before bFGF reduced ACE mRNA to approximately 50% of that found in the presence of bFGF alone.The results indicate that ACE mRNA is present in human vascular smooth muscle cells and that exposure to an ACE inhibitor reduces DNA synthesis. Basic FGF stimulates DNA synthesis and ACE mRNA expression, and both of these effects are reduced by an ACE inhibitor. The results are consistent with the effects of bFGF being exerted through, or alternatively in concert with, angiotensin II. Further, they suggest that ACE inhibition can reduce the activity of the renin-angiotensin system by inhibiting the production of ACE, or at least the expression of ACE mRNA, in addition to producing enzyme inhibition at the ACE level.

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Section: Introductionmentioning

confidence: 99%

ACE inhibition and fibroblast growth factor in cultured human vascular smooth muscle

1999

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“…Even though it is widely believed that circulating Ang II is the major player in regulating vascular myogenic tone, many recent studies also suggested that all components of the RAS pathway can be found locally in the blood vessels. Renin was reported to be found in cultured smooth muscle cells in rats and arterial cells in humans, yet its expression and activity in vivo remains controversial (27,28). Other RAS components, including AGT, ACE, and Ang II, were found within the endothelium of conduit arteries, resistance vessels, and veins (29)(30)(31).…”

Section: Pathway and Functionmentioning

confidence: 99%