Effect of pressure overload and its recovery on the rat carotid artery: change of vascular reactivity and remodeling process

Kwon, Jin-Sook; Lee, Sang-Jin; Kim, Young-Gyu; Bae, Jang‐Whan; Hwang, Kyung‐Kuk; Cho, Myeong Chan; Kim, Dong Ho

doi:10.1007/s00380-005-0861-5

Cited by 7 publications

(2 citation statements)

References 21 publications

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“…The increases in arterial thickness and cross-sectional area in this study are similar to those measured in rats with induced hypertension (8,16,33,35) and in humans with hypertension (26). In response to increased pressure, both ELN ϩ/ϩ and ELN ϩ/Ϫ ascending aortas are remodeled to increase the thickness and cross-sectional area and, consequently, to normalize the circumferential wall stress.…”

Section: Unloaded Dimensions Of the Ascending Aorta And Carotid Arterysupporting

confidence: 81%

Elastin-insufficient mice show normal cardiovascular remodeling in 2K1C hypertension despite higher baseline pressure and unique cardiovascular architecture

Wagenseil

Knutsen

Li³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Mice heterozygous for the elastin gene (ELN(+/-)) show unique cardiovascular properties, including increased blood pressure and smaller, thinner arteries with an increased number of lamellar units. Some of these properties are also observed in humans with supravalvular aortic stenosis, a disease caused by functional heterozygosity of the elastin gene. The arterial geometry in ELN(+/-) mice is contrary to the increased thickness that would be expected in an animal demonstrating hypertensive remodeling. To determine whether this is due to a decreased capability for cardiovascular remodeling or to a novel adaptation of the ELN(+/-) cardiovascular system, we increased blood pressure in adult ELN(+/+) and ELN(+/-) mice using the two-kidney, one-clip Goldblatt model of hypertension. Successfully clipped mice have a systolic pressure increase of at least 15 mmHg over sham-operated animals. ELN(+/+) and ELN(+/-)-clipped mice show significant increases over sham-operated mice in cardiac weight, arterial thickness, and arterial cross-sectional area with no changes in lamellar number. There are no significant differences in most mechanical properties with clipping in either genotype. These results indicate that ELN(+/+) and ELN(+/-) hearts and arteries remodel similarly in response to adult induced hypertension. Therefore, the cardiovascular properties of ELN(+/-) mice are likely due to developmental remodeling in response to altered hemodynamics and reduced elastin levels.

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Section: Unloaded Dimensions Of the Ascending Aorta And Carotid Arterysupporting

confidence: 81%

Elastin-insufficient mice show normal cardiovascular remodeling in 2K1C hypertension despite higher baseline pressure and unique cardiovascular architecture

Wagenseil

Knutsen

Li³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…Recent studies have shown that there is a myocardial inflammatory reaction and fibrotic response after TAC 3 and inflammatory signalling pathways are considered to be important in heart failure 4 and cardiac hypertrophy 5 . It has also been demonstrated that in addition to cardiac pathological changes, the right and left carotid arteries are modified differently with regard to morphology and function in the TAC model 6–9 . However, there are no studies on the effect of acute mechanical haemodynamic stimulus on aortic remodelling using this model.…”

Section: Introductionmentioning

confidence: 98%

Effect of an acute mechanical stimulus on aortic structure in the transverse aortic constriction mouse model

Chen

et al. 2011

Clin Exp Pharma Physio

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1. Vascular remodelling is an adaptive response to various stimuli, including mechanical forces, inflammatory cytokines and hormones. In the present study, we investigated histological modification of the aorta and the expression of key proteins participating in vascular remodelling under an acute mechanical stimulus using a transverse aortic constriction (TAC) mouse model. 2. The TAC was performed in male C57BL/6 mice aged 10-12 weeks. A Millar conductance catheter was used to measure cardiac haemodynamic parameters 3 and 14 days after TAC. Aortic structural variations were observed by haematoxylin and eosin, Sirius red and Weigert's elastin staining. Protein levels of Type I collagen, F4/80, α-smooth muscle actin (SMA) and SM22α were analysed by immunohistochemistry. 3. Three days after TAC, the medial area proximal to the aortic band (PA-B) was increased, whereas the area distal to the aortic band (DA-B) was unchanged. There was no difference in luminal area between TAC and sham groups. The adventitia displayed the most significant difference 14 days after TAC: adventitial hyperplasia was abundant and collagen was upregulated in the adventitia of the PA-B with a considerable increase in α-SMA and SM22α. Macrophages accumulated in the adventitia of the PA-B 3 days after TAC and infiltrated into the media and intima of the PA-B 14 days after TAC. 4. In conclusion, the aortic structure undergoes considerable remodelling following an acute mechanical stimulus in the TAC model, mainly in the adventitia. Upregulation of α-SMA and extracellular matrix components accompanied by macrophage infiltration may contribute to adventitial modification in the TAC mouse model.

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Favorable cardiac and aortic remodeling in olmesartan-treated spontaneously hypertensive rats

Fernandes-Santos

Mandarim-de-Lacerda

2009

Heart Vessels

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Cardiovascular remodeling contributes to the progression of cardiovascular disease. Thus, our aim was to evaluate the action of long-term treatment with olmesartan on cardiac and aortic adverse remodeling and its relationship with blood pressure (BP) and tensile forces acting on the aortic wall. Five-month-old male rats were divided in: WKY group (n = 6), SHR group (n = 6), and SHRs treated with hydralazine 30 mg/kg/day (SHR-H, n = 8) or olmesartan 10 mg/kg/day (SHR-O, n = 8). Medications were administered for 16 weeks. The SHR group showed hypertension (189 +/- 4 mmHg), cardiomyocyte hypertrophy (+107%), interstitial fibrosis (5.7% vs 1.9% in WKY), and reduced intramyocardial vascularization (9.1% vs 22.8% in WKY). In aorta, the SHRs showed outward hypertrophic remodeling, increased elastic fibers content (+36%), and increased circumferential wall tension (CWT, 2.79 x 10(4) dyne/cm) and tensile stress (TS, 261.4 x 10(4) dyne/cm(2)). Hydralazine and olmesartan decreased BP (-45% approximately) and likewise CWT and TS (-45% and -35% approximately). Both medications prevented left ventricle remodeling, but olmesartan improved cardiomyocyte hypertrophy better than hydralazine. Hydralazine did not alter media hypertrophy, but it enlarged lumen diameter and increased elastic fibers. It is unlikely that olmesartan prevented all aortic alterations. Taken together, long-term control of BP alone is not sufficient to prevent aortic remodeling due to hypertension, but in myocardium it seems to be enough, except for cardiomyocyte hypertrophy. The differential action of olmesartan suggests that it is essential to block growth stimulation by angiotensin II in cardiomyocytes and vascular smooth muscle cells in order to better prevent cardiovascular adverse remodeling due to arterial hypertension.

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Effect of pressure overload and its recovery on the rat carotid artery: change of vascular reactivity and remodeling process

Cited by 7 publications

References 21 publications

Elastin-insufficient mice show normal cardiovascular remodeling in 2K1C hypertension despite higher baseline pressure and unique cardiovascular architecture

Elastin-insufficient mice show normal cardiovascular remodeling in 2K1C hypertension despite higher baseline pressure and unique cardiovascular architecture

Effect of an acute mechanical stimulus on aortic structure in the transverse aortic constriction mouse model

Favorable cardiac and aortic remodeling in olmesartan-treated spontaneously hypertensive rats

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