beta-endorphins (beta-ends) are released from the anterior pituitary and from lymphocytes directly into inflamed tissue in response to stress and pain. At the site of inflammation and trauma, the link of beta- ends to opioid receptors hyperpolarizes nerve terminal, by blocking L-calcium gated channels, induces modifications of receptor stereoisomerism and alters the bond-energy. Opioids increase potassium and decrease calcium and sodium currents through interactions with G-protein. In some pathologies, it has been found a loss of desensitization and down regulation of opioid receptors by means of Ca++ blocking that, in turn, inhibits PKC-activation. The physiopathological mechanism dependent on the high concentration of linked opioids affects cellular level of Ca++, ATP and NADH. This biochemical reaction exerts deep influence on energetic cell status and metabolism. In gram negative bacteria, expression of mu-receptors on cell surface has been observed, with a possibility to interfere with host cell metabolism. There are many human and veterinary pathologies in which the reported mechanisms are well known: polycystic ovary syndrome, gross cystic breast disease, milk fever, ruminal tympanites, pyometra, equine colic syndrome, ovarian follicular cyst in dairy cows, calcium deficit in post-partum cows, uterine involution in cows. Also incoming pathologies such as Electro-Magnetic-Field exposure may induce alteration of calcium channel activity through the same mechanism. On clinical bases, it has been pointed out that the therapeutic administration of an association of calcium salts and naloxone controls calcium turnover, pain and functional activity of endocrine glands, via down regulation/desensitization of opioid receptors, PKC stimulation and energy restoration.