Effect of transport on pituitary responsiveness to exogenous pulsatile GnRH and oestradiol-induced LH release in intact ewes.
This study examined the effect of transport on GnRH self-priming in vivo as well as the consequential effects on the oestradiol-induced LH surge. The follicular phases of ewes (eight per group) were synchronized with progestin sponges, and 50 micrograms oestradiol benzoate was injected 24 h (time zero) after sponge removal to improve precision in the timing of the LH surge. Beginning 8 h after oestradiol, saline or GnRH (500 ng, i.v.) was given at 2 h intervals with or without 8 h transport beginning 0.5 h before the first GnRH injection (late transport) and effects were compared with those observed during early transport, that is, starting 2.5 h before the first GnRH injection. In all ewes, GnRH alone induced a maximum LH response of 1.9 +/- 0.4 ng ml-1 after the first challenge. The response was enhanced (P < 0.01) after the second and third GnRH injections (7.4 +/- 1.4 ng ml-1 and 7.6 +/- 1.7 ng ml-1, respectively). This self-priming effect after the second GnRH was reduced by late transport (7.4 +/- 1.4 versus 4.2 +/- 0.8 ng ml-1; P < 0.05) but not early transport, that is, transport initiated closer to the time of GnRH administration had greater suppressive effects on LH secretion. Throughout transport, spontaneous LH pulse frequency was lower in treated than it was in control ewes (2.38 +/- 0.53 versus 4.50 +/- 0.53 pulses per 8 h; P < 0.01), with marked effects in the first 4 h of transport (1.0 +/- 0.19 versus 2.63 +/- 0.38 pulses per 4 h; P < 0.02). Spontaneous pulse amplitude also tended to decrease during transport (0.13 +/- 0.02 versus 0.20 +/- 0.03 ng ml-1; P = 0.07). When LH turnover was stimulated by exogenous GnRH, the onset of the LH surge was delayed (controls: 20.5 +/- 2.0 h versus GnRH alone: 25.3 +/- 1.5 h; P < 0.05) and the duration was reduced (8.5 +/- 0.9 versus 6.5 +/- 0.4 h; P < 0.05). Transport tended to delay the LH surge in saline-treated ewes (20.5 +/- 2.0 versus 22.9 +/- 1.9 h; P = 0.08), with a further delay imposed by late transport plus GnRH (27.5 +/- 1.6 h; P < 0.05) but not by early transport plus GnRH (27.8 +/- 2.5 versus 26.4 +/- 2.4 h; P > 0.05), that is, effects mediated by increasing LH turnover were only manifest if transport occurred near the LH surge, when there was insufficient time to replenish stores of releasable LH. In all transported ewes, plasma cortisol increased from 4.5 +/- 1.0 ng ml-1 to 29.2 +/- 5.5 ng ml-1 (P < 0.001) within 15 min of the start of transport and was significantly lower (P < 0.01) by 6.5 h. Plasma progesterone also increased from 0.30 +/- 0.04 to 0.38 +/- 0.04 ng ml-1 (P < 0.05). In conclusion, transport affected the oestradiol-induced LH surge by causing a 50% reduction in the self-priming effect of exogenous GnRH, but hypothalamic effects were also revealed by a two-fold decrease in spontaneous LH pulse frequency in saline-treated ewes.
Phogat
J B
JB
Department of Veterinary Clinical Science and Animal Husbandry, University of Liverpool, Leahurst, Neston, South Wirral, UK.
Smith
R F
RF
Dobson
H
H
D000704:Analysis of Variance; D000818:Animals; D004958:Estradiol / Q000494:pharmacology*; D005260:Female; D005498:Follicular Phase; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology*; D006854:Hydrocortisone / Q000097:blood; D007247:Infertility, Female / Q000209:etiology* / Q000503:physiopathology; D007986:Luteinizing Hormone / Q000378:metabolism*; D008954:Models, Biological; D010902:Pituitary Gland / Q000187:drug effects* / Q000503:physiopathology; D011374:Progesterone / Q000097:blood; D012636:Secretory Rate / Q000187:drug effects; D012756:Sheep / Q000502:physiology*; D013268:Stimulation, Chemical; D013315:Stress, Psychological / Q000150:complications* / Q000503:physiopathology; D013997:Time Factors
D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone; D004958:Estradiol; D007986:Luteinizing Hormone; D006854:Hydrocortisone