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

100%

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

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.

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

80%

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

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.

Immunomodulatory effects of HMG-CoA reductase inhibitors

80%

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

Archivum Immunologiae et Therapiae Experimentalis

2003

tom 51

nr 3