Influence of catecholamines, prostaglandins and thyroid hormones on growth hormone secretion by chicken pituitary cells in vitro

Abstract In young chickens plasma concentrations of growth hormone (GH) are depressed by prostaglandins (PG) E 1 and E 2 , epinephrine, norepinephrine, α 2 and β agonists or thyroid hormones. A primary culture of chicken adenohypopyseal cells was used to examine the direct effects of these agents at the level of the pituitary as evaluated by GH release in the presence and absence of growth hormone releasing factor (GRF). Following collagenase dispersion and culture (preincubation, 48 hr) cells were exposed (incubation, 2 hr) to test agents, except for thyroid hormones which were added during the preincubation, and incubation period. Growth hormone release was increased (P 1 (10 −8 M by 34%; 10 −7 M by 54%), PGE 2 (10 −8 M by 29%; 10 −7 M by 29%), PGF 2α (10 −8 M by 28%), and the β agonist isoproterenol (10 −7 M by 46%). Basal GH release from chicken pituitary cells was not affected by dopamine, norepinephrine, epinephrine, thyroxine (T 4 ), triiodothyronine (T 3 ), or α adrenergic agonists. Growth hormone releasing factor stimulated GH release was not affected by the presence of prostaglandins E 1 , E 2 or F 2α in the incubation media. However, GRF stimulated GH release was reduced by high doses of catecholamines: dopamine (10 −6 M by 34%), norepinephrine (10 −6 M by 74%), epinephrine (10 −8 M by 47%; 10 −7 M by 41%; 10 −6 M by 89%), and by the α 1 adrenergic agonist, phenylephrine (10 −7 M by 52%), the α 2 agonist, clonidine (10 −8 M by 34%; 10 −7 M by 83%) and the β agonist, isoproterenol (10 −7 M by 64%). Similarly, GRF-induced GH release was decreased by coincubation with 10 or 100 ng/ml of T 3 by 75% and 89%, respectively. In contrast, T 4 did not affect GH release evoked by GRF although T 3 depressed GH release in the presence of both thyrotropin releasing hormone (TRH) and GRF. To determine the temporal relationship for T 3 inhibition of GRF stimulated GH release, T 3 (1.3 × 10 −8 M) was added during either the preincubation, incubation period or both. T 3 did not affect basal GH release during any time period, however, T 3 supplementation during the preincubation (48 hr) or both the preincubation (48 hr) and incubation (2 hr) period did suppress GRF stimulated GH release. These data suggest that the decrease in plasma concentration of GH observed in young chickens injected with catecholamines or T 3 may involve direct effects on the pituitary gland. However, the inhibitory effects of PGE 1 , PGE 2 and PGF 2α on in vivo GH secretion appears to be mediated at another site, presumably the hypothalamus.