Effects of carvedilol or amlodipine on target organ damage in L-NAME hypertensive rats: their relationship with blood pressure variability

Mauro, Julieta S. Del; Prince, Paula D.; Donato, Martín; Machulsky, Nahuel Fernandez; Morettón, Marcela A.; Gónzalez, Germán E.; Bertera, Facundo M.; Carranza, Andrea; Gorzalczany, Susana; Berg, Gabriela; Morales, Celina; Gelpi, Ricardo J.; Taira, Carlos A.; Höcht, Christián

doi:10.1016/j.jash.2017.02.007

Cited by 14 publications

(8 citation statements)

References 56 publications

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“…The rises in blood pressure promoted by L-NAME throughout early, middle and late pregnancy stages found in the present study are in accordance with previous reports [35,36,50,51]. Although we did not observe decreases in NO bioavailability in virgin and early-pregnant rats treated with L-NAME, our results regarding to the reduced NO bioavailability followed by increases in systolic blood pressure during middle and late pregnancy stages indicate that the demand for constitutive NOS isoforms-synthesized NO, i.e., by the endothelial (eNOS) and neuronal (nNOS), in the nanomolar range, may be increased at the later stages of pregnancy.…”

Section: Discussionsupporting

confidence: 94%

Reductions of Circulating Nitric Oxide are Followed by Hypertension during Pregnancy and Increased Activity of Matrix Metalloproteinases-2 and -9 in Rats

Nascimento

Possomato-Vieira

Bonacio

et al. 2019

Cells

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Hypertensive pregnancy has been associated with reduced nitric oxide (NO), bioavailability, and increased activity of matrix metalloproteinases (MMPs). However, it is unclear if MMPs activation is regulated by NO during pregnancy. To this end, we examined activity of MMP-2 and MMP-9 in plasma, placenta, uterus and aorta, NO bioavailability, oxidative stress, systolic blood pressure (SBP), and fetal-placental development at the early, middle, and late pregnancy stages in normotensive and Nω-Nitro-L-arginine methyl-ester (L-NAME)-induced hypertensive pregnancy in rats. Reduced MMP-2 activity in uterus, placenta, and aorta and reduced MMP-9 activity in plasma and placenta with concomitant increased NO levels were found in normotensive pregnant rats. By contrast, increased MMP-2 activity in uterus, placenta, and aorta, and increased MMP-9 activity in plasma and placenta with concomitant reduced NO levels were observed in hypertensive pregnant rats. Also, elevated oxidative stress was displayed by hypertensive pregnant rats at the middle and late stages. These findings in the L-NAME-treated pregnant rats were also followed by increases in SBP and associated with fetal growth restrictions at the middle and late pregnancy stages. We concluded that NO bioavailability may regulate MMPs activation during normal and hypertensive pregnancy.

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Section: Discussionsupporting

confidence: 94%

Reductions of Circulating Nitric Oxide are Followed by Hypertension during Pregnancy and Increased Activity of Matrix Metalloproteinases-2 and -9 in Rats

Nascimento

Possomato-Vieira

Bonacio

et al. 2019

Cells

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“…The overexpression of MMP-mediated vascular remodeling was stimulated by oxidative stress and inflammatory cytokines [ 54 ]. Del Mauro and coworkers demonstrated that MMP-2 and MMP-9 activity was a pathologic process in l -NAME-induced morphometric alterations in the aorta [ 55 ]. Interestingly, the authors of the present study first reported l -NAME-induced hypertension and vascular remodeling in rats in which there was an up-regulation of MMP-2 and MMP-9 protein expression in response to oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Hesperidin Prevents Nitric Oxide Deficiency-Induced Cardiovascular Remodeling in Rats via Suppressing TGF-β1 and MMPs Protein Expression

et al. 2018

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Hesperidin is a major flavonoid isolated from citrus fruits that exhibits several biological activities. This study aims to evaluate the effect of hesperidin on cardiovascular remodeling induced by n-nitro l-arginine methyl ester (l-NAME) in rats. Male Sprague-Dawley rats were treated with l-NAME (40 mg/kg), l-NAME plus hesperidin (15 mg/kg), hesperidin (30 mg/kg), or captopril (2.5 mg/kg) for five weeks (n = 8/group). Hesperidin or captopril significantly prevented the development of hypertension in l-NAME rats. l-NAME-induced cardiac remodeling, i.e., increases in wall thickness, cross-sectional area (CSA), and fibrosis in the left ventricular and vascular remodeling, i.e., increases in wall thickness, CSA, vascular smooth muscle cells, and collagen deposition in the aorta were attenuated by hesperidin or captopril. These were associated with reduced oxidative stress markers, tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta 1 (TGF-β1), and enhancing plasma nitric oxide metabolite (NOx) in l-NAME treated groups. Furthermore, up-regulation of tumor necrosis factor receptor type 1 (TNF-R1) and TGF- β1 protein expression and the overexpression of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) was suppressed in l-NAME rats treated with hesperidin or captopril. These data suggested that hesperidin had cardioprotective effects in l-NAME hypertensive rats. The possible mechanism may involve antioxidant and anti-inflammatory effects.

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“…Carvedilol is a beta-blocker, and there is ample evidence that Carvedilol has a beneficial effect on left ventricular systolic dysfunction (LVSD) after MI [31] and gives priority to improving the REDOX status of the heart and can prevent cardiac dysfunction and REDOX imbalance after MI [32]. e latest randomized controlled double-blind clinical trial also demonstrated that Carvedilol significantly reduced cardiac troponin levels and diastolic dysfunction [33] and reduced biomarkers of tissue fibrosis and inflammation in hypertensive disease models, such as TGFβ [34]. erefore, using Carvedilol as positive control can ensure the effectiveness of the Wenxin granule compound in the experiment.…”

Section: Discussionmentioning

confidence: 99%

Wenxin Granules Influence the TGFβ-P38/JNK MAPK Signaling Pathway and Attenuate the Collagen Deposition in the Left Ventricle of Myocardial Infarction Rats

Lou

et al. 2019

Cardiology Research and Practice

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Background. A large number of proinflammatory/anti-inflammatory cytokines are produced in the extracellular matrix (ECM) after myocardial infarction (MI), and the inflammatory pathways activated by these inflammatory stimuli are involved in the regulation of lesions with excessive accumulation of ECM. Wenxin granules can play a protective role against MI, but the mechanism of its effect on the inflammatory pathway and ECM collagen expression is still unclear. Objective. To verify the effect of Wenxin granules on the inflammatory pathway and collagen expression after MI. Method. e proximal left anterior descending coronary artery in rats was ligated to induce acute MI. en, animals were randomly assigned to the model group, the Carvedilol group, and the Wenxin Granules group. In addition, sham operation rats were used as the control group. 10 rats were allocated in each group. Gavage was given once a day for 4 weeks. e changes of cardiac hemodynamics were detected by the catheter method, morphological changes were observed by HE staining, and myocardial tissue collagen volume was counted by Immunohistochemistry combined with Masson staining, and the expression of inflammatory TGFβ-p38/JNK MAPK signal pathway markers was detected by Western blot. Results. Wenxin granules could significantly improve the hemodynamics, so that the fibrosis scar was relatively dense and uniform, and the residual myocardium was relatively neat, while Collagen type I and III volume and TGFβ expression levels were lessened. Although there were no differences in the expression of CTGF, p38, and JNK proteins, their phosphorylation levels showed significant differences. Conclusion. Wenxin granules can affect the inflammationrelated TGFβ-p38/JNK MAPK signaling pathway and change the structural properties of myocardium and scar after MI by attenuated collagen deposition in the left ventricular myocardial tissue to improve cardiac function.

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Effects of carvedilol or amlodipine on target organ damage in L-NAME hypertensive rats: their relationship with blood pressure variability

Cited by 14 publications

References 56 publications

Reductions of Circulating Nitric Oxide are Followed by Hypertension during Pregnancy and Increased Activity of Matrix Metalloproteinases-2 and -9 in Rats

Reductions of Circulating Nitric Oxide are Followed by Hypertension during Pregnancy and Increased Activity of Matrix Metalloproteinases-2 and -9 in Rats

Hesperidin Prevents Nitric Oxide Deficiency-Induced Cardiovascular Remodeling in Rats via Suppressing TGF-β1 and MMPs Protein Expression

Wenxin Granules Influence the TGFβ-P38/JNK MAPK Signaling Pathway and Attenuate the Collagen Deposition in the Left Ventricle of Myocardial Infarction Rats

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