Abstract
It is well known that immobilization stress for two hours decrease blood calcium levels via the gastric vagus-gastrin-histamine pathway, however, effects of other types of stress comditions and possible hypocalcemic factors are not well studies. Since neurochemical pathway to induce gastric acid secretion has been shown to share the hypocalcemic pathway, ghrelin and thyrotropin-releasing factor, peripheral and central gastric acid secreting agents are the possible candidates to induce hypocalcemia. In the present study, the effects of electrical shock (1 mA, 3 s/min 10 times), 2-buten-4-olide (2-B4O), ghrelin and TRH on blood ionized calcium levels were examined using male Wistar rats. 2-B4O is the fasting-induce anorectic agents which facilitates hypothalamo-pituitary-adrenal axis indicating a possible metabolic stress agent. Electrical shock but not psychological stress in the communication box induced hypocalcemia 15 min after initiation of stresses. Intravenous (IV) or intracerebroventricular (ICV) injection of ghrelin (0.05, 0.5, 5μg) did not affect blood calcium levels but IV and ICV injection of TRH (2, 20, 200μg) decreased blood calcium levels. 2-B4O was ineffective to induce hypocalcemia. The present study suggests that the ghrelin not take part though TRH had the possibility of taking part in the stress low calcium blood syndrome though the ghrelin and TRH were central acid in the stomach secretion promotion both factors. [J Physiol Sci. 2007;57 Suppl:S165]
