19 Interaction of kisspeptin and the somatotropic and lactotropic axes in mares and geldings

Abstract

Several experiments were conducted to investigate the interaction between kisspeptin and the somatotropic and lactotropic axes in mares and geldings. Light horse, diestrous mares and geldings, weighing approximately 500 kg and aged 6 to 24 years, were randomly assigned to treatment with 1 mg equine kisspeptin-10 (Kp10; n = 10) or 1 mL saline (n = 9), i.v. Blood samples were collected via jugular venipuncture −10, 0, 5, 10, 15, 20 and 30 min relative to treatment. Plasma concentrations of growth hormone (GH) and prolactin (PRL) were determined by RIA and means compared using ANOVA with repeated sampling. Neither GH nor PRL were stimulated by Kp10. In a second experiment, 30 mares and geldings were used to determine if pre-treatment with estradiol or progesterone would elicit a GH or PRL response to Kp10. Five mares and 5 geldings each were assigned to pre-treatment with 50 mg estradiol cypionate in oil (ECP), 600 mg long-acting progesterone, or oil only, i.m. Two days later, all horses received 1 mg Kp10 in saline, i.v., and blood sampling occurred 0, 5, 10, 15 and 20 min relative to Kp10 administration. Mean GH and PRL concentrations and area under the curve were compared by ANOVA. No stimulation of GH or PRL was observed. In a third experiment, 12 diestrous mares, confirmed by plasma progesterone and ultrasound findings, were randomly assigned to treatment with 1 mg Kp10 (n = 6) or 1 mL saline (n = 6) followed by the dopamine antagonist, sulpiride (0.01 mg/kg body weight), 5 min later. Blood sampling occurred 0, 5, 10 and 15 min relative to sulpiride administration. Sulpiride stimulated PRL ( P < 0.0001) in both groups of mares; however, PRL concentrations were lower ( P ≤ 0.01) in Kp10-treated mares compared with saline-treated mares. To determine if estrogen altered the PRL response to sulpiride, 12 seasonally anovulatory mares, confirmed by plasma progesterone and ultrasound findings, were used in a fourth experiment and randomly assigned to receive 50 mg ECP (n = 6) or oil (n = 6), i.m. The next day, mares were challenged with sulpiride. Treatment and blood sampling occurred as described in experiment 3. Plasma PRL was stimulated ( P < 0.001) in both groups of mares and responses were similar between treatments. In the described experiments, 1 mg Kp10 given as a bolus failed to stimulate circulating GH or PRL within 30 min in mares or geldings regardless of steroid milieu. This is in contrast to reports of GH stimulation in ruminants. Kp10 did alter the PRL response to sulpiride in diestrous mares, perhaps suggesting an interaction between Kp10 and dopaminergic input to the pituitary in a progesterone dominant environment.