Wyniki wyszukiwania

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The role of perivascular adipose tissue and endogenous hydrogen sulfide in vasoactive responses of isolated mesenteric arteries in normotensive and spontaneously hypertensive rats

100%

Cacanyiova S., Majzunova M., Golas S., Berenyiova A.

Journal of Physiology and Pharmacology

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2019

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tom 70

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nr 2

2

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Properties of ventricular myocytes isolated from the hypertrophied and failing hearts of spontaneously hypertensive rats

100%

Emanuel K., Mackiewicz U., Pytkowski B., Lewartowski B.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 2

3

Peroxisome proliferator-activated receptor alpha is downregulated in the failing human heart

100%

Karbowska J., Kochan Z., Smolenski R. T.

Cellular and Molecular Biology Letters

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2003

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tom 08

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nr 1

Cardiac hypertrophy in humans is associated with a decrease in myocardial fatty acid β-oxidation (FAO) and accompanying alterations in metabolic gene expression. Flux through the cardiac FAO pathway, which is the principal source of energy production in the adult mammalian heart, is tightly controlled in accordance with energy demands. In rodents, the FAO pathway is under control of a nuclear peroxisome proliferator-activated receptor α (PPARα). We sought to delineate the molecular regulatory events involved in the energy substrate preference switch from fatty acids to glucose during cardiac hypertrophic growth in humans. We analysed the amount of PPARα protein in human cardiac tissue. PPARα protein level was measured in homogenates prepared from left ventricular biopsies taken from five control donor hearts and compared to the amount of this transcription factor in biopsies from five patients with compensated end-stage heart failure (HF) at the time of transplantation. Using Western blot analysis with a monoclonal antibody against human PPARα, we observed a significant decrease (54%) in the mean amount of PPARα in the group of HF patients compared to that in the donor tissue. This study indicates that the decrease in cardiac PPARα transcription factor gene expression observed in the failing human heart could play an important role in a reduction in fatty acid utilisation by the adult heart during cardiac hypertrophy.

4

Chronic NG-nitro-l-arginine methyl ester (L-NAME) administration in C57BL/6J mice induces a sustained decrease in c-kit positive cells during development of cardiac hypertrophy

80%

Ocsan R. J., Lai Y. N., Prabhu K. V., Hambly B. D., McLachlan

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 6

5

Isoproterenol induces in vivo functional and metabolic abnormalities; similar to those found in the infarcted rat heart

80%

Heather L. C., Catchpole A. F., Stuckey D. J., Cole M. A., Carr C. A., Clarke K.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 3

31-39

Chronic isoproterenol administration produces a rapid, highly reproducible rodent model of cardiac hypertrophy. Yet, despite widespread use of this model, the effects of isoproterenol on in vivo cardiac function and substrate metabolism are unknown. Isoproterenol (5 mg.kg-1.day-1) was infused for 7 days in male Wistar rats (n = 22). In vivo magnetic resonance imaging (MRI) showed that left ventricular mass increased by 37% and end-diastolic and systolic volumes increased by 33% and 73%, respectively, following isoproterenol infusion. Cardiac function at the base of the left ventricle was normal, but apical ejection fraction decreased from 90% to 31% and apical free wall thickening decreased by 94%, accompanied by increased fibrosis and inflammation. Myocardial palmitate oxidation rates were 25% lower, and citrate synthase and medium chain acyl-coenzyme A dehydrogenase activities were reduced by 25% and 29%, respectively, following isoproterenol infusion. Fatty acid transporter protein levels were 11-52% lower and triglyceride concentrations were 55% lower in isoproterenol-infused rat hearts. Basal glycolysis and glycogen concentration were not changed, yet insulin stimulated glycolysis was decreased by 32%, accompanied by 33% lower insulin stimulated glucose transporter, GLUT4, protein levels in rat hearts following isoproterenol infusion, compared with controls. In conclusion, isoproterenol infusion impaired in vivo cardiac function, induced hypertrophy, and decreased both fatty acid and glucose metabolism, changes similar in direction and magnitude to those found in the rat heart following moderate severity myocardial infarction.

6

Effects of calcium sensitizer OR-1896 on cardiovascular mortality and myocardial remodelling in hypertensive Dahl/Rapp rats

80%

Louhelainen M., Merasto S., Finckenberg P., Vahtola E., Kaheinen P., Leskinen H., Levijoki J., Pollesello P., Haikala H., Mervaala E. M. A.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 3

41-47

Calcium-sensitizing agents have been shown to improve cardiac function in patients suffering from acute decompensated heart failure, however, their long-term effects on cardiac remodeling and cardiovascular mortality are still largely unknown. In the present study we tested the hypothesis whether OR-1896, an active and long-lasting metabolite of calcium sensitizer levosimendan, prevents cardiovascular mortality and hypertension-induced myocardial remodelling in salt-sensitive Dahl/Rapp rats. OR-1896 was given orally to Dahl/Rapp SS rats on high-salt diet (NaCl 7% w/w) for 7 weeks at two different doses (0.5 and 0.05 mg/kg). OR-1896 prevented salt-induced cardiovascular mortality (survival rate 75 % in OR-1896 treated groups vs 38 % in untreated controls, p<0.01), ameliorated cardiac hypertrophy and improved systolic functions of the heart without major influence on systemic blood pressure. OR-1896 also ameliorated salt-induced increase in cardiac ANP mRNA expression and plasma BNP level. Salt-induced cardiac remodelling was associated with 4-fold increase in cardiac p16INK4a mRNA expression, a marker of cellular senescence. OR-1896 dose-dependently ameliorated cardiomyocyte senescence. Our findings suggest a therapeutic role for OR-1896 in the prevention of cardiac remodelling in salt-sensitive forms of hypertension. The present study also underscores the importance of cellular senescence in the pathogenesis of salt-induced hypertensive heart disease.

7

Cardioprotection of exogenous erythropoietin in mice with ligature-induced aortic stenosis: effects on maladaptive cardiac hypertrophy

80%

Zheng L., Xu J., Qiu W., Liu X., Zhao C.-M., Chen D., Chen Y.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 1

13-20

Pre-operative treatment with recombinant human erythropoietin may improve aortic stenosis patients' condition, including anemia and/or cardiac dysfunction, for subjecting to aortic valve replacement. In this study, we tested this hypothesis in a mouse model of aortic stenosis. Adult male mice were subjected to either aortic stenosis created by aortic ligature or sham operation. Aortic stenosis for 4 weeks caused cardiac hypertrophy, pulmonary congestion and left ventricular dysfunction. It was associated with increased levels of tumor necrosis factor-a in serum and myocardium, and reduced levels of interleukin-10 in myocardium but not in serum. Mytocyte apoptosis rate, level of cleaved caspase 3, activity of nuclear factor-B and expression of p38-MAPK pathway were also elevated. Erythropoietin treatment increased hematocrit but did not prevent the development of cardiac hypertrophy. It, however, reduced the apoptosis, prevented the increases in tumor necrosis factor-, nuclear factor-B activation and phosphorylation of p38, and attenuated the increases in lung weight, the decreases in LVEF and LVFS, and the increases in LVDd and LVDs. In conclusion recombinant human erythropoietin has cardioprotective effects in maladaptive cardiac hypertrophy by inhibiting nuclear factor-B activation, phosphorylation of p38-MAPK pathway, and production of tumor necrosis factor-, together leading to a reduced apoptosis.

8

Cardiac effects of osteostatin in mice

80%

Meyer R., Schreckenberg R., Kraus D., Kretschmer F., Schulz R., Schluter K.-D.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 1

9

Enhanced expression of mineralocorticoid receptors in the heart after the myocardial infarct in rats

80%

Milik E., Szczepanska-Sadowska E., Maslinski W., Cudnoch-Jedrzejewska A.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 4

Increasing evidence suggests that enhanced stimulation of the heart and kidney by mineralocorticoids plays significant role in development of the post-infarct cardiac failure. Because increased synthesis of mineralocorticoid receptors (MR) is one of the putative factors determining pathogenic effects of mineralocorticoids we decided to determine whether the myocardial infarct results in an enhanced expression of MR mRNA and MR protein. To this end male Sprague-Dawley rats were subjected either to ligation of the left coronary artery or to sham surgery. After four weeks expressions of MR mRNA and MR protein were evaluated in both groups of rats in the left (LV) and right (RV) ventricle walls, and in the renal cortex and renal medulla by means of semiquantitative PCR and Western blotting methods. Coronary ligation resulted in the myocardial infarction encompassing 30.2% ± 1.9% (range 23-40%) of the left ventricle wall. In the infarcted rats expression of MR mRNA was significantly greater than in the sham-operated rats, both in the LV (P<0.02) and in the RV (P<0.005). In the left but not in the right ventricle increased MR mRNA expression was associated with significant increase in expression of MR protein (P<0.001). In the renal cortex and renal medulla MR mRNA and MR protein expression in the infarcted and the sham-operated rats did not differ. The study reveals that during the post-infarct state expression of MR mRNA is elevated in both cardiac ventricles while expression of MR mRNA protein is increased only in the left ventricle. The results suggest that the enhanced expression of mineralocorticoid receptors may contribute to enhanced effects of mineralocorticoids in the heart during the post-infarct state.

Ograniczanie wyników

The role of perivascular adipose tissue and endogenous hydrogen sulfide in vasoactive responses of isolated mesenteric arteries in normotensive and spontaneously hypertensive rats

Properties of ventricular myocytes isolated from the hypertrophied and failing hearts of spontaneously hypertensive rats

Peroxisome proliferator-activated receptor alpha is downregulated in the failing human heart

Chronic NG-nitro-l-arginine methyl ester (L-NAME) administration in C57BL/6J mice induces a sustained decrease in c-kit positive cells during development of cardiac hypertrophy

Isoproterenol induces in vivo functional and metabolic abnormalities; similar to those found in the infarcted rat heart

Effects of calcium sensitizer OR-1896 on cardiovascular mortality and myocardial remodelling in hypertensive Dahl/Rapp rats

Cardioprotection of exogenous erythropoietin in mice with ligature-induced aortic stenosis: effects on maladaptive cardiac hypertrophy

Cardiac effects of osteostatin in mice

Enhanced expression of mineralocorticoid receptors in the heart after the myocardial infarct in rats