title: Growth hormone and prolactin secretion in hypophysial stalk-transected pigs as affected by growth hormone and prolactin-releasing and inhibiting factors.
abstract: Control of growth hormone (GH) and prolactin (PRL) release was investigated in hypophysial stalk-transected (HST) and stalk-intact pigs by determining the effects of analogs of GH-releasing factors (GHRF), somatostatin (SRIF), arginine, thyrotropin-releasing hormone, alpha-methyl-rho-tyrosine, and haloperidol. HST and control gilts were challenged with intravenous injections of human pancreatic GHRF(1-40)OH, thyrotropin-releasing hormone, and analogs of rat hypothalamic GHRF. HST animals remained acutely responsive to GHRF by releasing 2-fold greater quantities of GH than seen in controls. This occurred in spite of a 38% reduction in pituitary gland weight and a 32 and 55% decrease in GH concentration and total content. During SRIF infusion, GH remained at similar basal concentrations in HST and control gilts, but increased immediately after stopping SRIF infusion only in the controls. Releasable pituitary GH appears to accumulate during SRIF infusion. GHRF given during SRIF infusion caused a 2-fold greater release of GH than seen in animals receiving only GHRF. Arginine increased (P less than 0.05) GH release in controls, but not in HST gilts, which suggests that it acts through the central nervous system. Basal PRL concentrations were greater (P less than 0.05) in HST gilts than in control gilts. TRH acutely elevated circulating PRL (P less than 0.001) in HST gilts, suggesting that it acts directly on the pituitary gland. Haloperidol, a dopamine receptor antagonist, increased circulating PRL in controls but not in HST animals. alpha-Methyl-rho-tyrosine did not consistently increase circulating PRL, however, suggesting that it did not sufficiently alter turnover rate of the tyrosine hydroxylase pool. The results indicate that the isolated pituitary after HST remains acutely responsive to hypothalamic releasing and inhibiting factors for both GH and PRL release in the pig.
authors.affiliation: Department of Animal Science, Iowa State University, Ames 50011.
authors.forename: L L
authors.initials: LL
authors.lastname: Anderson
authors.forename: J J
authors.initials: JJ
authors.lastname: Ford
authors.forename: J
authors.initials: J
authors.lastname: Klindt
authors.forename: J R
authors.initials: JR
authors.lastname: Molina
authors.forename: W W
authors.initials: WW
authors.lastname: Vale
authors.forename: J
authors.initials: J
authors.lastname: Rivier
mesh_terms: D000311:Adrenal Glands / Q000033:anatomy & histology; D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001835:Body Weight; D005260:Female; D013006:Growth Hormone / Q000031:analogs & derivatives / Q000378:metabolism*; D013007:Growth Hormone-Releasing Hormone / Q000494:pharmacology; D006220:Haloperidol / Q000494:pharmacology; D006221:Halothane / Q000494:pharmacology; D007016:Hypophysectomy; D008781:Methyltyrosines / Q000494:pharmacology; D009929:Organ Size; D010902:Pituitary Gland / Q000502:physiology*; D011388:Prolactin / Q000031:analogs & derivatives / Q000378:metabolism*; D011863:Radioimmunoassay; D013004:Somatostatin / Q000494:pharmacology; D013552:Swine; D013961:Thyroid Gland / Q000033:anatomy & histology; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology; D014446:Tyrosine 3-Monooxygenase / Q000037:antagonists & inhibitors; D019805:alpha-Methyltyrosine
chemical_list: D008781:Methyltyrosines; D013004:Somatostatin; D013973:Thyrotropin-Releasing Hormone; D019805:alpha-Methyltyrosine; D011388:Prolactin; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone; D001120:Arginine; D014446:Tyrosine 3-Monooxygenase; D006220:Haloperidol; D006221:Halothane