Wyniki wyszukiwania

1

Changes of cardiovascular mortality in rural areas in Hungary

100%

Sumegi G., Komlosi M., Tenyi J.

Annals of Agricultural and Environmental Medicine

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1994

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tom 01

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nr 2

2

A new membrane G protein-coupled receptor (GPR30) is involved in the cardiac effects of 17beta-estradiol in the male rat

63%

Filice E., Recchia A. G., Pellegrino D., Angelone T., Maggiolini M., Cerra M. C.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 4

3-10

In the present study, we evaluated the transduction pathways involved in the cardiac effects elicited by 17ß-estradiol (E2) on the isolated, Langendorff perfused male Wistar rat heart. E2 and selective agonists for ER and ERß induced a dose-dependent reduction of contractility which was blocked by the ER inhibitor ICI 182,780. Moreover, the potential involvement of the novel membrane estrogen receptor GPR30 in mediating estrogen activity was determined using the selective GPR30 ligand G-1. Notably, specific inhibitors of ERK, PI3K, PKA, and eNOS transduction pathways abolished the cardiac responses to E2. Taken together, our data suggest that ER and ERß along with several signaling cascades are involved in the action of E2 on the male rat heart. Our results also point to a potential role of GPR30, however further evaluation is required in order to fully understand the contribution of the different estrogen receptors in mediating estrogen activity on cardiac performance.

3

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

51%

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.

4

Immunomodulatory effects of HMG-CoA reductase inhibitors

51%

Danesh F. R., Anel R. L., Zeng L., Lomasney J., Sahai A., Kanwar Y. S.

Archivum Immunologiae et Therapiae Experimentalis

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2003

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tom 51

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nr 3

5

Detrimental effects of testosterone on post-myocardial infarction remodeling in female rats

51%

Frantz S., Hu K., Widder J., Weckler B., Scheuermann H., Bauersachs J., Ertl G., Callies F., Allolio B.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 4

Clinical data suggest an association of increased serum androgens with cardiovascular mortality in females, but not in males. Therefore, we examined effects of chronic anabolic testosterone administration on left ventricular remodeling after myocardial infarction in female rats. Ovariectomized adult female rats were treated with placebo, supraphysiologic testosterone undecanoate (T), estradiol (E2), or T+E2. Two weeks after ovarcectomy, animals underwent sham-operation or coronary artery ligation. Left ventricular remodeling and function were assessed by echocardiography and hemodynamic investigation. In sham operated animals T administration increased serum T levels and led to cardiac hypertrophy, with an increase in the ß/alpha-MHC-ratio and in IGF-1 expression. After coronary artery ligation, infarct size and mortality were similar among the groups. T treatment aggravated left ventricular hypertrophy and chamber dilatation (end-diastolic diameter, E2 vs. T vs. E2+T, 8.6 ± 0.6 vs. 9.9 ± 0.3 vs. 9.8 ± 0.3 mm, p<0.05) and reduced fractional shortening 8 weeks after myocardial infarction. Extracellular matrix remodeling was not altered by hormonal treatment. In conclusion, chronic anabolic T treatment causes myocardial hypertrophy under basal conditions and adversely affects left ventricular remodeling following myocardial infarction in female rats.

Ograniczanie wyników

Changes of cardiovascular mortality in rural areas in Hungary

A new membrane G protein-coupled receptor (GPR30) is involved in the cardiac effects of 17beta-estradiol in the male rat

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

Immunomodulatory effects of HMG-CoA reductase inhibitors

Detrimental effects of testosterone on post-myocardial infarction remodeling in female rats