Modulation of vascular development and injury by angiotensin II

Hutchinson, Howard G.; Hein, Lutz; Fujinaga, Masahiko; Pratt, Richard E.

doi:10.1016/s0008-6363(98)00267-3

Cited by 49 publications

(52 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Activation of AT 2 has been associated with vasodilator effects (Tscho¨pe et al, 2002) and AT 2 receptors re-expresssion was reported to occur 48-72 h after injury (Hutchinson et al, 1999). This effect may be the consequence of an increased production of inducible nitric oxide in the ipsilateral vessel wall, as suggested by several studies (Major et al, 1985;Joly et al, 1992;Douglas et al, 1994;Hansson et al, 1994).…”

Section: Accorsi-mendonc¸a Et Al Vascular Change In Distant Uninjumentioning

confidence: 93%

“…Ang II stimulates DNA synthesis in the media and neointima after angioplasty (Hutchinson et al, 1999). Powell et al (1989) and others (Hanson et al, 1991;Farhy et al, 1992;Rakugi et al, 1994;Fernandez-Alfonso et al, 1997) reported that angiotensinconverting enzyme inhibitors or AT 1 antagonist are able to prevent balloon-induced neointima formation in rats.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrine

Accorsi‐Mendonça¹,

Corrêa²,

Paiva

et al. 2004

British J Pharmacology

View full text Add to dashboard Cite

1 The effects of balloon injury on the reactivity of ipsilateral and contralateral carotid arteries were compared to those observed in arteries from intact animals (control arteries). 2 Carotid arteries were obtained from Wistar rats 2, 4, 7, 15, 30 or 45 days after injury and mounted in an isolated organ bath. Reactivity to angiotensin II (Ang II), phenylephrine (Phe) and bradykinin (BK) was studied. Curves were constructed in the absence or presence of endothelium or after incubation with 10 mM indomethacin, 500 mM valeryl salicylate or 0.1 mM celecoxib. 3 Phe, Ang II and BK maximum effects (Emax) were decreased in ipsilateral arteries when compared to control arteries. No differences were observed among pD2 or Hill coefficient. 4 Emax to Phe (4 and 7 days) and to Ang II (15 and 30 days) increased in the contralateral artery. In addition, Phe or Ang II reactivity was not significantly different in aorta rings from control or carotid-injured animals. 5 The increased responsiveness of contralateral artery was not due to changes in carotid blood flow or resting membrane potential. The endothelium-dependent inhibitory component is not present in the contraction of contralateral arteries and it is not related to superoxide anion production. 6 Indomethacin decreased contralateral artery responsiveness to Phe and Ang II. Valeryl salicylate reduced the Ang II response in contralateral and control arteries. Celecoxib decreased the Phe Emax of contralateral artery. 7 In conclusion, decreased endothelium-derived factors and increased prostanoids appear to be responsible for the increased reactivity of contralateral arteries after injury.

show abstract

Section: Accorsi-mendonc¸a Et Al Vascular Change In Distant Uninjumentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

The balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrine

Accorsi‐Mendonça¹,

Corrêa²,

Paiva

et al. 2004

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Although the physiological relevance of Ang II in endothelial cells (ECs) remains to be fully elucidated, the significant roles of Ang II in EC growth and proliferation as well as apoptosis are well known (5,6). Given that Ang II has been associated with the regulation of endothelium-dependent vascular relaxation in the rabbit aorta and rat coronary artery, it is reasonable to hypothesize that its vasoconstrictive effects on VSMC may be counterbalanced by its concurrent effects on ECs via its regulation of the release of NO (7,8).…”

Section: Introductionmentioning

confidence: 99%

Effects of Angiotensin II on Nitric Oxide Generation in Proliferating and Quiescent Rat Coronary Microvascular Endothelial Cells

Bayraktutan

Ülker

2003

Hypertens Res

View full text Add to dashboard Cite

phospholipases C and D or protein kinase C (2). These transducers in turn regulate the expression of several growth factors, including platelet-derived growth factor and basic fibroblast growth factor (3). In contrast, AT2 is expressed in a few adult tissues, such as heart and kidney tissues, at low levels, and its activation has been implicated in growth inhibitory and/or proapoptotic effects as a result of stimulation of tyrosine phosphatase(s) (4). The results of recent studies suggest that co-stimulation of the AT2 receptor along with blockade of the AT1 receptor by either Ang II receptor blockers or angiotensin converting enzyme inhibitors (ACEIs) increases nitric oxide (NO) release and causes some

show abstract

“…release of angiotensin ii (anG ii) in response to vascular injury plays an important role in neointimal hyperplasia through the stimulation of VSMc proliferation and migration (8,9). Two distinct subtypes of anG ii receptors, type 1 (AT1R) and type 2 (AT2R), have been identified.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of angiotensin II type 2 receptor suppresses neointimal hyperplasia in a rat carotid arterial balloon injury model

Tang

Yang

et al. 2011

Mol Med Rep

View full text Add to dashboard Cite

Abstract. angiotensin ii (anG ii) type 2 receptor (aT2r) has been recognized to suppress the proliferation of vascular smooth muscle cells (VSMcs). The aim of the present study was to determine whether aT2r overexpression inhibits neointimal hyperplasia in a rat carotid arterial balloon injury model and to examine the underlying mechanisms of its activity. Balloon-injured rats receiving ad-aT2r showed significant diminutions in neointimal area and intima/ media ratio compared to non-treated rats or rats receiving adenovirus containing green fluorescent protein (Ad-GFP). In addition, extracellular regulated kinase 1/2 (ERK1/2) and basic transcription element-binding protein 2 (BTeB2) were significantly down-regulated in the arteries and VSMCs of Ad-AT2R-treated rats and compared to Ad-GFP-treated rats. However, ad-aT2r transfection failed to affect the expression of anG ii type 1 receptor (aT1r) in carotid arteries and cultured VSMcs. The present study provides direct evidence that AT2R plays a beneficial role in balloon injury-induced neointimal hyperplasia, which is mainly attributed to the inhibition of VSMc proliferation and involves the down-regulation of the ERK1/2 and BTEB2 pathways, but is independent of the expression of aT1r. IntroductionPercutaneous transluminal balloon angioplasty is widely used for the treatment of obstructed atherosclerotic vascular diseases (1). However, balloon injury to the arterial wall induced by restenosis limits its overall benefits (2). Despite dramatic advances in reducing the incidence of restenosis by drug-eluting stents, it remains a considerable medical challenge (3-5). The major pathological process underlying restenosis is neointimal hyperplasia (6), which results from the phenotypic modulation, proliferation, migration and extracellular matrix synthesis of vascular smooth muscle cells (VSMcs) (7).release of angiotensin ii (anG ii) in response to vascular injury plays an important role in neointimal hyperplasia through the stimulation of VSMc proliferation and migration (8,9). Two distinct subtypes of anG ii receptors, type 1 (AT1R) and type 2 (AT2R), have been identified. The proliferation effect of anG ii has been attributed to aT1r (10,11). additionally, treatment with aT1r blockers (arBs) reduces the incidence of restenosis (12,13). aT2r is expressed abundantly in the fetal vasculature with rapid decline after birth, and is re-expressed in the adult vasculature under certain pathological cardiovascular conditions, such as vessel injury and inflammation (14,15). In injured vessels, aT1r is highly expressed, while aT2r is expressed at low levels (16). Furthermore, it has been reported that aT2r has anti-proliferation, anti-migration and proapoptotic effects on VSMcs in vitro, and antagonizes the growth effect of aT1r (17,18). These lines of evidence suggest that aT2r plays a crucial role in the neointimal hyperplasia response to vascular injury.in this study, we investigated the effects of the overexpression of aT2r by adenoviral gene transfer on neointimal hyperpla...

show abstract

Modulation of vascular development and injury by angiotensin II

Abstract: These results indicate that Ang II receptors play a role in vascular development by promoting opposing effects on vascular smooth muscle cell growth.

Cited by 49 publications

References 39 publications

The balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrine

The balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrine

Effects of Angiotensin II on Nitric Oxide Generation in Proliferating and Quiescent Rat Coronary Microvascular Endothelial Cells

Overexpression of angiotensin II type 2 receptor suppresses neointimal hyperplasia in a rat carotid arterial balloon injury model

Contact Info

Product

Resources

About