EN
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.