Aim. The present study was designed to investigate the effects of estradiol-ethylenediamine derivative on perfusion pressure and coronary resistance in rats. An additional aim was to identify the molecular mechanisms involved. Methods. The Langendorff model was used to measure perfusion pressure and coronary resistance changes in isolated rat heart after estradiol-ethylenediamine derivative alone and following compounds; tamoxifen (estrogen receptor antagonist), prazosin (alpha1 adrenoreceptor antagonist), metoprolol (selective beta1 receptor blocker), indomethacin (prostanglandin synthesis inhibitor) and nifedipine (L-type calcium-channel inhibitor). Results. The results show that estradiol-ethylenediamine derivative [10–9 mmol] significantly increased perfusion pressure (p= 0.005) and coronary resistance (p= 0.006) in isolated rat heart. Additionally, the effect of estradiolethylenediamine on perfusion pressure [10–9 to 10–4 mmol] was only blocked in the presence of the L-type calciumchannel (nifedipine).

Conclusions. These data suggest that the effect of estradiol-ethylenediamine on perfusion pressure and vascular coronary involves activation of the L-type calcium channel through a non-genomic molecular mechanism.