科研之友
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摘要
Corticotropin releasing hormone (CRH) plays a central role in regulating the release of adreno-corticotropic hormone (ACTH) during a stress response. ACTH acts on the adrenal glands, inducing the secretion of cortisol. In our previous study, we reported that ACTH administration to ovariectomized gilts results in the plasma elevation of cortisol, progesterone and prostaglandin F2汐 metabolite [15]. How ACTH is capable of stimulating the secretion of PGF2汐 metabolite remains unanswered. However, it was previously suggested by [8] that ACTH enhances the conversion in vitro of 3H-arachidonic acid to prostaglandins in feline adrenocortical cells. The findings of [2] indicate that prostaglandins in the brain interact in their stimulatory regulation of ACTH secretion. Such an interaction may also be involved in prostaglandins mediation of the ACTH response to immunochallenges. [1] reported that stimulation of porcine pituitary cells by relatively low concentrations of prostaglandin E2 support increased secretion of ACTH but exposure to greater concentrations of this prostaglandin in fact suppresses ACTH secretion. Food deprivation, which is a form of stress, has been shown to result in the plasma elevation of both cortisol and PGF2汐 metabolite [24,11,14,17].Intracerebroventricular as well as intravenous injections of CRH resulted in an increased plasma cortisol concentration in pigs [20,7]. Previously, it was suggested that CRH may also act directly or indirectly to enhance cortisol secretion beyond the level achieved through adrenal stimulation by ACTH [12].The objectives of the present study were to evaluate the effects of synthetic ACTH (tetra-cosactid) and porcine CRH on the plasma levels of cortisol and PGF2汐 metabolite in cycling gilts and castrated boars.Six crossbred pigs (Landrace ℅ Yorkshire; three gilts and three castrated boars) aged approximately 6 months weighing between 110 and 125 kg were used for this experiment. The pigs were brought to the Division of Com
