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Eplerenone improves vascular function and reduces platelet activation in diabetic rats

100%

Schafer A., Vogt C., Fraccarollo D., Widder J., Flierl U., Hildemann S. K., Ertl G., Bauersachs J.

Journal of Physiology and Pharmacology

2010

tom 61

nr 1

45-52

Diabetes is associated with endothelial dysfunction and platelet activation, both of which contribute to increased cardiovascular risk. We investigated whether the selective mineralocorticoid receptor (MR) antagonist eplerenone improves endothelial dysfunction and reduces platelet activation in diabetic rats. Male Wistar-rats were injected with streptozotocin (50 mg/kg i.v.) to induce insulin-deficient diabetes. After 2 weeks, treatment with eplerenone (100 mg/kg/day) or vehicle was initiated for 2 weeks. Aortic superoxide production determined by lucigenin-enhanced chemiluminescence and 2-hydroxyethidium formation was significantly increased in rats with diabetes and reduced by treatment with eplerenone (chemiluminescence: control 2045±227, STZ-placebo 3977±340, p<0.05 vs. control, STZ-eplerenone 1762±307, p<0.05 vs. STZ-placebo). Endothelium-dependent vasorelaxation was significantly attenuated in diabetic rats and was normalized by eplerenone (maximum relaxation in % of precontraction: control 95±3, STZ-placebo 82±3, p<0.01 vs. control, STZ-eplerenone 99±1, p<0.01 vs. STZ-placebo). Treatment with the selective MR antagonist significantly reduced fibrinogen-binding on activated GPIIb/IIIa (immunofluorescence: control 161±7, STZ-placebo 208±16, p<0.05 vs. control, STZ-eplerenone 173±6, p<0.05 vs. STZ-placebo). Eplerenone improves endothelial function by reducing superoxide formation and increasing NO bioavailability in diabetic rats. Platelet activation was significantly reduced by eplerenone. Selective MR blockade may constitute a useful therapeutic approach for treatment of vascular dysfunction in diabetes.

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

100%

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

Journal of Physiology and Pharmacology

2007

tom 58

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

2 Journal of Physiology and Pharmacology

2 Bauersachs J.

2 Ertl G.

2 Widder J.

1 Allolio B.

1 Callies F.

1 Flierl U.

1 Fraccarollo D.

1 Frantz S.

1 Hildemann S. K.

1 Hu K.

1 Schafer A.

1 Scheuermann H.

1 Vogt C.

1 Weckler B.

1 2010

1 2007

Wyniki wyszukiwania

Eplerenone improves vascular function and reduces platelet activation in diabetic rats

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