Abstract

The present study was designed to evaluate the effects of synthetic ACTH (1–24, tetracosactid) and porcine CRH on the plasma levels of cortisol and PGF2α metabolite in cycling gilts (n = 3) and castrated boars (n = 3). The experiments were designed as crossover studies for each gender separately. Each animal received, during three consecutive days; 1) ACTH (Synacthen® Depot) at a dose of 10 μg/kg body weight in 5 ml physiological saline, 2) porcine CRH at a dose 0.6 μg/kg body weight in 5 ml physiological saline or 3) physiological saline (5 ml). The test substances were administered via an indwelling jugular cannula in randomized order according to a Latin square. The administration of ACTH to cycling gilts resulted in concomitant elevations of cortisol and PGF2α metabolite with peak levels reached at 70.0 ± 10.0 and 33.3 ± 6.7 min, respectively. Similarly, the administration of ACTH to castrated boars resulted in concomitant elevation of cortisol and PGF2α metabolite with peak levels reached at 60.0 ± 0.0 and 20.0 ± 0.0 min, respectively. Cortisol peaked at 20 min after administration of CRH in both cycling gilts and castrated boars with maximum levels of 149.3 ± 16.5 nmol/1 and 138.3 ± 10.1 nmol/1, respectively. It can be concluded that administration of synthetic ACTH (tetracosactid) to pigs caused a concomitant elevation of cortisol and PGF2α metabolite levels in both cycling gilts as well as castrated boars. The administration of CRH to pigs resulted in an elevation of cortisol levels in both cycling gilts and castrated boars. Conversely, PGF2α metabolite levels were not influenced by the administration of CRH either in cycling gilts or in castrated boars.

Highlights

  • Corticotropin releasing hormone (CRH) plays a central role in regulating the release of adrenocorticotropic hormone (ACTH) during a stress response

  • PGF2α metabolite levels were not influenced by the administration of CRH either in cycling gilts or in castrated boars

  • The administration of ACTH to cycling gilts resulted in concomitant elevations of cortisol (Figure 1) and PGF2α metabolite (Figure 2) with peak levels reached at 70.0 ± 10.0 and 33.3

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Summary

Introduction

Corticotropin releasing hormone (CRH) plays a central role in regulating the release of adrenocorticotropic hormone (ACTH) during a stress response. We reported that ACTH administration to ovariectomized gilts results in the plasma elevation of cortisol, progesterone and prostaglandin F2α metabolite (Mwanza et al 2000b). How ACTH is capable of stimulating the secretion of PGF2α metabolite remains unanswered It was previously suggested by Laychok & Rubin (1975) that ACTH enhances the conversion in vitro of 3H-arachidonic acid to prostaglandins in feline adrenocortical cells. It was suggested that CRH may act directly or indirectly to enhance cortisol secretion beyond the level achieved through adrenal stimulation by ACTH (Minton & Parsons 1993). The objectives of the present study were to evaluate the effects of synthetic ACTH (tetracosactid) and porcine CRH on the plasma levels of cortisol and PGF2α metabolite in cycling gilts and castrated boars

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