Modulatory effect of gonadal steroids on stress-induced endorphin release in ischemic rabbit heart

Beta-endorphins [BE] were recently detected in the heart. Since the incidence of cardiac disease in premenopausal females is by far less frequent than males and since opioid peptides were found to be affected by sex hormones in the CNS, the aim of this study was to investigate whether they also modulate the BE-response to acute stress in the isolated rabbit hearts subjected to ischemia and reperfusion injury. Stressed rabbits were divided into male and female groups with and without naloxone and castrated males and tamoxifen [estrogen-receptor blocker] pretreated females with and without naloxone. BE was found to have a cardioprotective effect during stress which is sex-related. It has a negative chronotropic and inotropic effect. It prolongs the time until cardiac arrest during ischemia and reduces reperfusion arrhythmia. However, the presence of testosterone has a detrimental effect on the cardiac response to stress, which may be due to inhibition of BE release. In addition, testosterone directly decreases contractility and shortens the duration until cardiac arrest during ischemia. It probably causes coronary vasoconstriction. Estrogen, on the other hand, possess protective properties in ischemic stressed heart and prevents reperfusion arrhythmia independent of BE. The effects of estrogen may be caused by a direct action or by release of opioid peptides, which act via non- mu-receptors

Effects of Norplant [subdermal implants] on serum levels of beta-endorphin: prolactin and gonadotropin

50 parous women were enrolled in a longitudinal study of the effect of Norplant subdermal [long acting levonorgestrel] implant on serum levels of gonadotropins [FSH and LH], prolactin [PRL] and beta- endorphin [beta-Ed] for 5 years user. All of them had children. 40 women only completed the study. 10 married parous women not using hormonal contraception volunteers as control. The Norplant users and the control were similarly studied. Starting by day 5 of their cycle until the next menses, three samples were taken [postmenstrual, midcycle and premenstrual phases]. These samples were collected at the end of one, two up to five years since insertion of Norplant. There was definite improvement in the bleeding pattern with time. Marked inhibition were noticed in the serum levels of LH and FSH surge during the first three years, then elevated to be in the range of normal levels in the last two years. Serum PRL and beta-Ed levels lost there normal cyclicity and sustained at a low or high tonic levels all over the study. This study suggested that, Norplant acts mainly by inhibiting the ovulation through suppressing the LH and FSH surge while, the anovulation may be the cause of cesation of normal pulsatility for both serum beta-Ed and PRL