Specific differences in cardiovascular diseases are largely mediated by sex hormones. Moreover, the use of estrogens significantly reduces the overall incidence of heart diseases in postmenopausal women. Beneficial effects of estrogens on plasma lipoprotein levels are clearly established. However, these do not explain the magnitude of risk reduction seen in clinical studies. Thus additional and currently unknown function of estrogens must be operative. The present work investigated the effect of (10-7-10-4 M) 17ß-estradiol concentrations on cardiac cell contraction. In addition, contraction measurements were further conducted on isoprenaline pre-stimulated cells. Finally, to find out the exact effect of the estradiol in both sets of experiments, separate experimental runs were performed using the ethanol concentrations added to the buffer during experimentation. Data were digitized, recorded, analyzed, normalized and processed with different programs sets. The obtained results showed that 17ß-estradiol has induced an inhibition effect on the contraction of myocytes starting from the lower concentration (10-7 M) used. Percentage inhibition recorded was 16.5%. In experiments using isoprenaline as a prestimulator, contraction measurements results demonstrated that the application of isoprenaline caused a mean increase in the peak value by 60.0%. After the onset of the lowest ß-estradiol concentration, decreased peak value measured was 8.6%. It was concluded that 17ß-estradiol has a negative inotropic effect on guinea-pig ventricular myocytes by inhibiting the Ca2⁺ current and so reducing systolic [Ca2⁺]i. 17ß-estradiol may therefore have a Ca2⁺ channel blocking property. Although the concentrations needed to gain this Ca2⁺ antagonistic influence were much too high to explain a cardioprotective influence of estrogen, it will probably enhance the therapeutic repertoire in treating heart diseases, the most common cause of death nowadays.
Key words: Contraction, 17ß-estradiol, myocytes, E-C coupling, guinea pig
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