Thyrotropin releasing hormone interactions with growth hormone secretion in horses.
Light horse mares, stallions, and geldings were used to 1) extend our observations on the thyrotropin releasing hormone (TRH) inhibition of GH secretion in response to physiologic stimuli and 2) test the hypothesis that stimulation of endogenous TRH would decrease the normal rate of GH secretion. In Exp. 1 and 2, pretreatment of mares with TRH (10 microg/kg BW) decreased (P < 0.001) the GH response to exercise and aspartate infusion. Time analysis in Exp. 3 indicated that the TRH inhibition lasted at least 60 min but was absent by 120 min. Administration of a single injection of TRH to stallions in Exp. 4 increased (P < 0.001) prolactin concentrations as expected but had no effect (P > 0.10) on GH concentrations. Similarly, 11 hourly injections of TRH administered to geldings in Exp. 5 did not alter (P > 0.10) GH concentrations either during the injections or for the next 14 h. In Exp. 5, it was noted that the prolactin and thyroid-stimulating hormone responses to TRH were great (P < 0.001) for the first injection, but subsequent injections had little to no stimulatory effect. Thus, Exp. 6 was designed to determine whether the inhibitory effect of TRH also waned after multiple injections. Geldings pretreated with five hourly injections of TRH had an exercise-induced GH response identical to that of control geldings, indicating that the inhibitory effect was absent after five TRH injections. Retrospective analysis of pooled, selected data from Exp. 4, 5, and 6 indicated that endogenous GH concentrations were in fact lower (P < 0.01) from 45 to 75 min after TRH injection but not thereafter. In Exp. 7, 6-n-propyl-2-thiouracil was fed to stallions to reduce thyroid activity and hence thyroid hormone feedback, potentially increasing endogenous TRH secretion. Treated stallions had decreased (P < 0.01) concentrations of thyroxine and elevated (P < 0.01) concentrations of thyroid-stimulating hormone by d 52 of feeding, but plasma concentrations of GH and prolactin were unaffected (P > 0.10). In contrast, the GH response to aspartate and the prolactin response to sulpiride were greater (P < 0.05) in treated stallions than in controls. In summary, TRH inhibited exercise- and aspartate-induced GH secretion. The duration of the inhibition was at least 1 h but less than 2 h, and it waned with multiple injections. There is likely a TRH inhibition of endogenous GH episodes as well. Reduced thyroid feedback on the hypothalamic-pituitary axis did not alter basal GH and prolactin secretion.
Pruett
H E
HE
Department of Animal Sciences, Louisiana Agricultural Experiment Station, Louisiana State University Agricultural Center, Baton Rouge 70803-4210, USA.
Thompson
D L
DL
Cartmill
J A
JA
Williams
C C
CC
Gentry
L R
LR
D000818:Animals; D019540:Area Under Curve; D001224:Aspartic Acid / Q000494:pharmacology; D005260:Female; D013006:Growth Hormone / Q000037:antagonists & inhibitors / Q000097:blood / Q000378:metabolism*; D006736:Horses / Q000097:blood / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011388:Prolactin / Q000097:blood*; D011897:Random Allocation; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism / Q000494:pharmacology*
D001224:Aspartic Acid; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D013006:Growth Hormone