Effects of angiotensin II and vasopressin on human smooth muscle cells in vitro

Campbell-Boswell, Mark; Robertson, Abel L.

doi:10.1016/0014-4800(81)90066-6

Cited by 300 publications

(115 citation statements)

References 15 publications

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“…Ang II is produced locally in the vascular wall and cultured VSMC (Dzau et al, 1983), and stimulates VSMC proliferation, which is a characteristic feature of vascular-related diseases such as atherosclerosis (Campbell-Boswell and Robertson, 1981;Geisterfer and Owens, 1989;Newby and George, 1993). Overproduction of Ang II accelerates the development of abnormal vascular wall thickening and atherosclerotic lesions in the vessels (Campbell-Boswell and Robertson, 1981;Geisterfer and Owens, 1989;Newby and George, 1993).…”

Section: Discussionmentioning

confidence: 99%

Catechins inhibit angiotensin II-induced vascular smooth muscle cell proliferation via mitogen-activated protein kinase pathway

Sun-Mi

Park²,

Kim³

et al. 2006

Exp Mol Med

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Section: Discussionmentioning

confidence: 99%

Catechins inhibit angiotensin II-induced vascular smooth muscle cell proliferation via mitogen-activated protein kinase pathway

Sun-Mi

Park²,

Kim³

et al. 2006

Exp Mol Med

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“…Angiotensin II inhibits mesangial cell collagenase activity [7] and these effects can be blocked by Losartan [7], an angiotensin II receptor blocker. Angiotensin converting enzyme in-hibitors reduce fibronectin [8] and matrix metalloproteinase [9] production of mesangial cells exposed to high glucose.…”

Section: :82-88]mentioning

confidence: 99%

Juxtaglomerular apparatus T-cell infiltration affects glomerular structure in Type 1 diabetic patients

2004

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Aims/hypothesis. Type 1 diabetes is an autoimmune disorder associated with T-cell mediated injury to multiple endocrine tissues. T-cell infiltration of the juxtaglomerular apparatus could be associated with changes in local renin angiotensin system activity and, thus, with changes in the renal microenvironment. We examined the frequency of juxtaglomerular apparatus T-cell infiltration early in Type 1 diabetes and tested whether this is associated with renal structure and function. Methods. We classified 89 Type 1 diabetic patients by immunohistochemical analysis as either juxtaglomerular apparatus T-cell positive (n=37) or T-cell negative (n=38). Borderline cases (n=14) were not considered further.Results. T-cell positive patients had a shorter duration of diabetes (6.7±2.5 years) than T-cell negative patients (9.2±5.0 years, p=0.011) and lower albumin excretion rate, but they had a similar glomerular filtration rate and blood pressure. Renal biopsy morphometric analysis showed similar glomerular basement membrane width and mesangial fractional volume in these two groups. However, glomerular capillary surface density (p=0.0012) and filtration surface per glomerulus (p=0.0155) were greater in the T-cell positive patients. Conclusion/Interpretation. Increased filtration surface per glomerulus could be associated with glomerular filtration rate preservation in diabetes. Thus, juxtaglomerular apparatus immunologic injury in Type 1 diabetes patients could delay the clinical consequences of diabetic nephropathy. [Diabetologia (2004) Minneapolis, MN 55455, USA E-mail: mauer002@umn.edu Abbreviations: ECM, Extracellular matrix; RAS, renin-angiotensin-system; JGA, juxtaglomerular apparatus; NHDN, natural history of diabetic nephropathy; IP, immunoperoxidase; GV, mean glomerular volume; TGF-B, transforming growth factor-B; Vv(Mes/glom), mesangial fractional volume per glomerulus; GBM, glomerular basement membrane; Sv(PGBM/glom), surface density of the peripheral glomerular capillary perglomerulus ; TFS, total filtration surface per glomerulus; Vv(Int/cortex), fractional volume of renal cortical interstitium.

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“…The stimulation of smooth muscle cells in culture by ANG II, however, had somewhat controversial effects. Whereas some authors also described hyperplastic effects of ANG II on vascular smooth muscle cells (221), other studies detected a hypertrophic response only (222,223). This apparent discrepancy can possibly be explained by species variability and differences in the experimental conditions.…”

Section: Vasculaturementioning

confidence: 94%

The Role of the Renin-Angiotensin System in Cardiovascular Disease.

et al. 1994

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Recent findings have increased our understanding of the role of the renin-angiotensin system in cardiovascular diseases. This was possible by the progress made in molecular biology and the import of this methodology into cardiovascular research by several groups in the past few years. Studies by these groups accumulated evidence especially for the existence and physiological importance of organ-based renin-angiotensin systems and their involvement in the pathogenesis of hypertension and the accompanying disorders of the heart, the kidney, and the vessels. This Review will focus mainly on the relevance of the local renin-angiotensin systems for cardiovascular diseases and the value of transgenic animals as models to analyse these systems (Hypertens Res 1994; 17: 1-16).

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Effects of angiotensin II and vasopressin on human smooth muscle cells in vitro

Cited by 300 publications

References 15 publications

Catechins inhibit angiotensin II-induced vascular smooth muscle cell proliferation via mitogen-activated protein kinase pathway

Catechins inhibit angiotensin II-induced vascular smooth muscle cell proliferation via mitogen-activated protein kinase pathway

Juxtaglomerular apparatus T-cell infiltration affects glomerular structure in Type 1 diabetic patients

The Role of the Renin-Angiotensin System in Cardiovascular Disease.

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