Prolactin and GH are produced by acidophil cells that are most abundant in the antero-lateral area of anterior pituitary
On the basis of AA percentage GH has complementary or antagonistic action with Prolactin?
Factors activating GH/Prolactin release
| Factors | GH | Prolactin |
| Dopamine | = | - |
| Histamine | = | + |
| Serotonine | = | + |
| Dopamine | = | - |
| Dopamine | = | - |
prolactin+histamine
Thymosin fraction 5
Thymosin fraction 5 stimulates prolactin and growth hormone release from anterior pituitary cells in vitro. 1987
- Thymosin fraction 5 (TF5) is a partially purified extract of bovine thymus containing 40-60 peptides. In addition to its well documented immunopotentiating effects, TF5 reportedly modulates the secretion of some hypothalamic peptides and pituitary hormones.
Galanin evokes a cytosolic calcium bursting mode and hormone release in GH3/B6 pituitary cells. 1990
- GH and PRL release during short term (4 h) incubations of P0 cells and primary cultures of dispersed rat pituitary cells was initially measured in response to GRF, TRH, vasoactive intestinal peptide (VIP), and SRIF.
[Studies on the secretion of human placental lactogen from human trophoblastic tissues (author's transl)]. 1982
- In order to study the secretory mechanism of human placental lactogen (hPL:hCS) from trophoblastic tissues, tissue culture and new placental perifusion systems were developed and used to clarify the effect of various substances on the secretion of hPL. These substances were (1), metal ions([Ca2+], [K+], [mg2+], [Na+]); (2) growth hormone and prolactin releasing or inhibiting factors (arginine, TRH, somatostatin, dopamine); (3) LH-RH, dibutyryl cyclic-AMP which stimulates hCG secretion; (4) prostaglandins F2 alpha and E2, bradykinin; (5) EGF and insulin which have the receptors in the placenta; (6) glucose. It was found that most of the substances examined had no effect on the secretion of hPL, except dopamine and glucose. The effect of dopamine in the tissue culture system is dose-dependent. At high concentrations dopamine slightly inhibited hPL secretion(5mM: 38.6 +/- 15.0 and 10mM; 35.7 +/- 19.0 micrograms/g wet tissue) compared with the control (63.2 +/- 29.8 microgram/g wet tissue). However, these effects may be due to the deviation of pH in the medium from the direct addition of dopamine hydrochloride. At a low concentration(1mM) it was observed to have a rather stimulatory effect (125.7 +/- 18.0 micrograms/g wet tissue, p less than 0.05), but in the perifusion system, this effect could not be observed. The addition of glucose in the perifusion system gave a slightly higher hPL secretion than that of the control. Perhaps this resulted from increased cell activity rather than a stimulatory effect. an incorporation experiment of [3H] leucine was also carried out to study the biosynthesis of hPL. Newly synthesized ([3H]-labelled) hPL was secreted into the medium within two hours. Furthermore, a labelled larger molecular weight substance together with the tritiated hPL was also observed on a Sephadex G-100 gel chromatography. These labelled substances were immunoprecipitable using an anti-hPL serum, indicating that the substances contain the same immunological determinants. This result indicates that the larger molecular substance may represent the biosynthetic precursor or the aggregate of hPL. These data indicate that the secretion of hPL has a unique mechanism, different from GH and PRL, and may be self regulated.
Involvement of alpha-adrenergic mechanisms in growth hormone release induced by opioid peptides in conscious rats. 1981
- On the other hand, GH release induced by FK 33-824 was not influenced by propranolol (1 mg/100 g b.w., i.v.), a beta-adrenergic blocking agent, nor pimozide (0.1 mg/100 g b.w., i.v.), a dopamine antagonist.
Beta-adrenergic stimulation of adenosine-3',5'-monophosphate (c-AMP) accumulation and of prolactin and growth hormone secretion in rat anterior pituitary cell cultures. 1985
- Stimulation of PRL and GH release from these cultures was also induced by the adenylyl cyclase activator forskolin.
Factors inhibiting GH/Prolactin release
Involvement of nitric oxide in the interferon-gamma-induced inhibition of growth hormone and prolactin secretion in anterior pituitary cell cultures. 1997
- The inhibition of PRL and GH release by IFN-gamma was markedly reduced in L-arginine-depleted medium.
MtTW-10 pituitary tumor cells: galanin gene expression and peptide secretion. 1993
- We investigated their modulation by 17 beta-estradiol (E2) and their involvement in dopamine (DA) and somatostatin (SRIF) inhibition of PRL and GH release.
Nafazatrom, an arachidonate metabolism inhibitor, decreases prolactin and GH release. 1986
- Nafazatrom, an inhibitor of arachidonate metabolism by the lipoxygenase enzymes, decreases basal prolactin and growth hormone release in a concentration-dependent manner without significantly affecting the synthesis of either hormone.
Arachidonic acid-induced hormone release in somatotropes: involvement of calcium. 1996
NGDA and ETYA reduced the effects of AA on GH release (50 and 74%, respectively) and inhibited the [Ca2+]i response, whereas indomethacin slightly potentiated both AA-induced GH release and [Ca2+]i increase.
The mechanism of action of cytokines to control the release of hypothalamic and pituitary hormones in infection. 2000
IL-1 alpha inhibits growth hormone (GH) release by inhibiting GH-releasing hormone (GHRH) release, which is mediated by NO, and stimulating somatostatin release, also mediated by NO.
Nitric oxide controls the hypothalamic-pituitary response to cytokines. 1997
IL-1 alpha inhibits growth hormone (GH) release by inhibiting GH-releasing hormone release mediated by NO and stimulating somatostatin release, also mediated by NO.
The role of nitric oxide (NO) in control of hypothalamic-pituitary function. 1996
The NOS diffuses to the LHRH terminal and activates guanylate cyclase (GC), cyclooxygenase and lipoxygenase causing release of LHRH via release of cyclic GMP, PGE2 and leukotrienes, respectively.
The role of nitric oxide (NO) in control of hypothalamic-pituitary function. 1996
The NOS diffuses to the LHRH terminal and activates guanylate cyclase (GC), cyclooxygenase and lipoxygenase causing release of LHRH via release of cyclic GMP, PGE2 and leukotrienes, respectively.
The metabolism and immunology of bone. 1989
Of the systemic factors, GH; somatomedin C (IGF-1); high concentrations of insulin, testosterone, PDGF and TGF beta;
Dopamine
"Endocrine rhythms in patients with restless legs syndrome. 2002":
Dopamine is the major inhibitory factor of prolactin release and also influences growth hormone (hGH) secretion.
Vitamin D, Pit-1, GH, and PRL: possible roles in breast cancer development.
Tetrahydropterin therapy for hyperphenylalaninemia caused by defective synthesis of tetrahydrobiopterin. 1983
h4 Conflicting results
Verapamil: influence upon basal and stimulated rat growth hormone and prolactin release in vitro. 1983":http://www.ncbi.nlm.nih.gov/pubmed/6134290
- [3H]GH release from pituitary explants perifused in standard medium (GIBCO Minimum Essential Medium: 1.8 mM Ca2+) s transiently increased by 50 microM verapamil while [3H]PRL release is suppressed.
Influence of somatostatin on serum prolactin concentrations of cows during rest and milking. 1980
- Administration of somatostatin (SRIF) to lactating cows significantly increased basal, premilking serum concentrations of prolactin (PRL), and potentiated PRL release in response to milking and significantly reduced resting concentrations of growth hormone (GH).
Dopamine downregulates prolactin synthesis.
Hyperprolactinemia, a tool in treatment control of tetrahydrobiopterin deficiency: endocrine studies in an affected girl.
Tetrahydropterin therapy for hyperphenylalaninemia caused by defective synthesis of tetrahydrobiopterin.
Abstract Prolactin induces enhanced interferon gamma release in peripheral whole blood after stimulation with either PHA or LPS.
Elevated serum prolactin concentrations in phenylketonuric patients on a 'loose diet'.
DNA-remethylation around a STAT5-binding enhancer in the alphaS1-casein promoter is associated with abrupt shutdown of alphaS1-casein synthesis during acute mastitis.
Serotonin and acetylcholine affect the release of prolactin and growth hormone from pituitary glands of domestic fowl in vitro in the presence of hypothalamic tissue. 1984
- Anterior pituitary glands from broiler fowl were incubated alone or with hypothalamic tissue in medium containing either serotonin or serotoninergic drugs, acetylcholine or cholinergic drugs, and the release of prolactin (Prl) and growth hormone (GH) measured by homologous radioimmunoassays. The neurotransmitters and drugs affected the release of hormones from the pituitary gland only when hypothalamic tissue was also present. Serotonin and its agonist quipazine stimulated the release of Prl and inhibited release of GH in a concentration-related manner. The antagonist methysergide blocked the effects of serotonin and quipazine on Prl. Acetylcholine and its agonist pilocarpine also stimulated release of Prl and inhibited release of GH in a concentration-related manner. Atropine blocked these responses.*The results show that serotonin and acetylcholine affect pituitary hormone secretion by acting on the hypothalamus*. They may stimulate the secretion of a Prl releasing hormone and somatostatin.
Similarity to Insulin receptor of dopamin action (G-protein mediated)
Differential involvement of nitric oxide signaling in dopamine and PACAP stimulation of growth hormone release in goldfish.
Prolactin is inversely related to BH4, 2007
Reproductive experience modifies dopaminergic function, serum levels of prolactin, and macrophage activity in female rats. 2007
Prolactin and autoimmune diseases in humans.2007
