Inhibition of injury induced intimal hyperplasia by saralasin in rats

Pan, Xian-Mang; Nelken, Nicolas A.; Colyvas, Nicholas; Rapp, Joseph H.

doi:10.1016/0741-5214(92)90017-3

Cited by 17 publications

(6 citation statements)

References 23 publications

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“…It has been reported that all components of the reninangiotensin system were found in the blood vessel wall and ACE inhibitors effectively inhibited neointimal formation in the rat models of vascular injury [5,6]. The relevance of ACE to neointimal formation was confirmed again by the present study showing the significant inhibition of neointimal formation by captopril (10 mg/kg/day for 21 days) in balloon-injured rat carotid artery.…”

Section: Discussionsupporting

confidence: 76%

“…Consistent with these reports, it was also known that exogenous administration of angiotensin II potentiated experimental neointimal formation [4], suggesting that the renin-angiotensin system plays an important role in neointimal formation. Moreover, it was known that ACE inhibitors [5,6] and angiotensin II receptor antagonists [7,8] reduced neointimal formation in the rat model of arterial injury.…”

Section: Introductionmentioning

confidence: 99%

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Effects of SK-1080 on Intimal Thickening and Impaired Vascular Relaxation after Ballon Injury in Rats

2002

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We investigated the effects of SK-1080, a novel angiotensin AT₁ receptor antagonist, on neointimal proliferation in the rat carotid artery after balloon injury, together with its effects on the impaired endothelium-dependent vascular relaxation. SK-1080 (0.3 and 1.0 mg/kg/day) was orally administered in balloon-injured rats for 21 days (from 6 days before to 14 days after balloon injury). SK-1080 (1 mg/kg) exerted significant effects on three important parameters associated with the intimal thickening induced by balloon injury (50.0% reduction in neointimal area, 42.7% reduction in stenosis ratio and 69.1% increase in lumen/total area ratio). Acetylcholine-induced relaxation was significantly reduced in the balloon-injured carotid arteries (64.0 ± 9.1%), and this impairment of acetylcholine-induced relaxation was significantly restored by SK-1080 (maximal relaxation: 87.1 ± 6.5 and 88.6 ± 1.9% at 0.3 and 1.0 mg/kg, respectively, p < 0.05). However, the endothelial-independent, sodium nitroprusside-induced relaxation was clearly demonstrated and did not differ in carotid arteries from all treatment groups. Furthermore, acetylcholine-induced relaxation was completely inhibited by L-NAME but not by indomethacin. SK-1080 caused a slight hypotension 1 day before balloon injury (8.7%), which gradually returned to the baseline 6 and 13 days after balloon injury. These results suggest that SK-1080 may have therapeutic potential for the treatment of vascular diseases such as restenosis and atherosclerosis.

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Section: Discussionsupporting

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Effects of SK-1080 on Intimal Thickening and Impaired Vascular Relaxation after Ballon Injury in Rats

2002

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“…Based on findings that flow-mediated vasodilation in hypertensive humans is impaired14, we anticipated that remodeling in the GH would be impaired. However, we provide evidence to the contrary since hypertension per se did not restrict outward remodeling, and nor did it enhance inward remodeling.…”

Section: Discussionmentioning

confidence: 99%

Flow-Mediated Vascular Remodeling in Hypertension

Ibrahim

Berk

2009

Stroke

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Background and Purpose-Changes in shear and medial wall stress induced by blood flow contribute to vascular remodeling, but details of these relations remain undefined. We hypothesized that remodeling has a strong genetic component and that phenotypic responses to hemodynamic stress will differ among rat strains. Here, we characterized phenotypic traits related to carotid remodeling in the 2 rat strains that we previously showed the greatest difference in shear stress regulation: Genetically Hypertensive (GH) and Brown Norway (BN) rat strains. Methods-Left internal and external carotid arteries were ligated and blood flow was reduced in the left common (LCA) by 90% and increased in the right common carotid artery (RCA) by 60%. Rats were studied for up to 28 days after flow modification and carotid outer diameters were measured in vivo, and wall and luminal components by histomorphometry, to obtain indices of remodeling. Blood flow and pressure measurements were made at corresponding time points. Results-By day 28, remodeling in the GH was greater in response to high flow than in BN, and shear stress was normalized. In contrast, remodeling in the BN was greater in the low flow LCA than in GH. Media stress was greater in GH than BN for any value of carotid shear stress and remained relatively unchanged in low flow, but markedly increased in high flow remodeling. Importantly, pressure was not a major determinant of flow remodeling in these conditions. Conclusions-There are key differences in the ability of carotids in GH and BN rats to adhere to hemodynamic laws during vascular remodeling. GH rats exhibit intact regulatory mechanisms for increased, but not reduced, shear stress. Moreover, the ability to maintain physiological shear and media stresses during vascular remodeling in response to modified flow appears to be intrinsically "genetically" determined.

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“…In contrast, myointimal lesion formation following vessel injury involves both smooth muscle cell migration and proliferation (Owens and Reidy 198%;Schwartz et al 1986, f99Q;Schwartz and Reidy 1987). Angiotensin converting enzyme inhibitors, as well as angiotensin I1 (AII) receptor antagonists, have been shown to inhibit the development of medial hypertrophy in hypertension (Azuma et d. Clozel et d. 1991 ;Kauffman et d. 1991 ;Owens 1987;Pan et al 1992) as well as the accelerated proliferation of smooth muscle cells following vessel injury ( k u m a et Clozel et al 1991 ;Kauffman et al 1991;Osterrieder et d. 1991;Pan et al 1992;Powell et al 1989Powell et al , 1991. Moreover, it has been demonstrated that AII can stimulate hypertrophic as well as hyperplastic growth of cultured smooth muscle cells (Geisterfer and Owens 1989;Geisterfer et al 1988;Stouffer and Owens 1992;Berk et d. 1989;Itoh et d. 1993;Naftilan 1992;Schelling et a%.…”

Section: Vascular Growth Promoting Factorsmentioning

confidence: 96%

Pathophysiology of smooth muscle in hypertension

Lee¹,

Owens²,

Scott‐Burden³

et al. 1995

Can. J. Physiol. Pharmacol.

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Structural changes of the arteries in hypertension are determined by the unique genetics of the animals and by various growth promoters and growth inhibitors. Vascular smooth muscle cell growth promoting factors include fibroblast growth factor, platelet-derived growth factor, and vasoactive peptides such as norepinephrine, angiotensin II, and endothelin. Endothelial cells secrete three types of growth inhibiting factors. These are heparin--heparan sulfate, transforming growth factor beta, and nitric oxide. The effect of sympathetic innervation on vascular growth is probably dependent on its interaction with the renin-angiotensin system. In the mesenteric vascular bed, the elevated resistance in the arterial system is present in both the macroarteries and in the more distal microarteries and veins. Changes in resistance arteries include hypertrophy and reduction in outer diameter (remodelling). In the resistance arteries from human essential hypertensives, remodelling is the predominant finding. Long-term treatment with an angiotensin I converting enzyme inhibitor but not with a beta-blocker was effective in reversing this type of vascular change. Studies have suggested that in addition to angiotensin II, endothelin may play a role in vascular remodelling of resistance arteries.

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Inhibition of injury induced intimal hyperplasia by saralasin in rats

Cited by 17 publications

References 23 publications

Effects of SK-1080 on Intimal Thickening and Impaired Vascular Relaxation after Ballon Injury in Rats

Effects of SK-1080 on Intimal Thickening and Impaired Vascular Relaxation after Ballon Injury in Rats

Flow-Mediated Vascular Remodeling in Hypertension

Pathophysiology of smooth muscle in hypertension

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