Renin-Angiotensin System in Cultured Human Arterial Smooth Muscle Cells

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

doi:10.1097/00005344-198906144-00010

Cited by 6 publications

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“…Although inhibition of circulating ACE may mediate this phenomenon, a large body of evidence suggests that the tissue renin-angiotensin system present in the vasculature may be more important ( 12). Vascular smooth muscle cells (VSMC) express many components of the renin-angiotensin system including angiotensinogen (13) and ACE, as shown by the binding of ramiprilate (14), and conversion of angiotensin I to angiotensin 11 (15). It has become clear that ACE expression is dynamically regulated in a tissue-specific manner.…”

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Fibroblast growth factor stimulates angiotensin converting enzyme expression in vascular smooth muscle cells. Possible mediator of the response to vascular injury.

et al. 1995

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IntroductionAngiotensin converting enzyme (ACE) Angiotensin converting enzyme (ACE),' a zinc-containing dipeptidase, catalyzes the proteolytic cleavage of angiotensin I to angiotensin II (1). The generation of this physiologic pressor and vascular growth factor by ACE is believed to be of major importance in the maintenance of normal vascular tone. Angiotensin II also participates in angiogenesis (2), vascular remodeling (3), and the vascular response to injury (4). Expanding knowledge of the renin-angiotensin system suggests important roles for ACE in vascular diseases such as hypertension, atherosclerosis, and restenosis. ACE activity is widely expressed in a variety of tissues including pituitary, adrenal (5), kidney, intestine (6), heart (7), and macrophages (8). In the vasculature, ACE has been thought to be expressed predominantly on the luminal surface of the endothelial cell (9). The endothelium is believed to be the major site of angiotensin II generation from angiotensin I.The tissue renin-angiotensin system appears to be important in the vascular response to injury. Daemen (4) showed that administration of angiotensin II stimulated intimal cell proliferation. Other investigators have demonstrated that systemically administered ACE inhibitors significantly decrease intimal proliferation ( 10) or intimal mass ( 11 ) after balloon injury in the rat carotid and aorta. Although inhibition of circulating ACE may mediate this phenomenon, a large body of evidence suggests that the tissue renin-angiotensin system present in the vasculature may be more important ( 12). Vascular smooth muscle cells (VSMC) express many components of the renin-angiotensin system including angiotensinogen (13)

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Fibroblast growth factor stimulates angiotensin converting enzyme expression in vascular smooth muscle cells. Possible mediator of the response to vascular injury.

et al. 1995

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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.…”

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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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