SEARCH · PubMed Health

Results for “PITUITARY HORMONES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 361 records · Page 20Linked to original sources

PubMed1989

Cachectin alters anterior pituitary hormone release by a direct action in vitro.

Cachectin (tumor necrosis factor) is a powerful macrophage hormone released during infection, which circulates in blood to produce diverse effects in the organism. We examined the effect of cachectin on release of anterior pituitary hormones from either hemipituitaries or dispersed pituitary cells incubated in vitro. The action of cachectin on dispersed cells was demonstrable only after 2 hr of incubation. With this incubation time, the protein produced a dose-related stimulation of release of adrenocorticotropin (ACTH), growth hormone (GH), and thyrotropin (TSH), but not of prolactin (Prl), from both hemipituitaries and dispersed cells. The doses required for stimulation were low in the case of hemipituitaries, usually of the order of 10(-12) M, whereas they were higher by one or two orders of magnitude with the dispersed pituitary cells. This may be related either to loss of receptors for the protein during the dispersion procedure or to the fact that in the hemipituitary system cell interactions are facilitated because the cells are close to each other. In the dispersed cell system cachectin evoked a dose-related decrease in cyclic AMP content. Incubation with somatostatin lowered the cyclic AMP content of the cells and depressed GH output without altering output of TSH or Prl. When somatostatin and cachectin were incubated together with the cells, the suppression of cyclic AMP production was abolished; TSH and Prl release were stimulated, but the action of cachectin to stimulate GH release was blocked. The stimulation of Prl release by cachectin in the presence of somatostatin may be related to the elevation of cyclic AMP, a known stimulator of Prl release. The cyclooxygenase inhibitor indomethacin nearly completely blocked the stimulatory effect of cachectin on release of GH and TSH from dispersed pituitary cells but had only a slight and nonsignificant attenuating effect on its ACTH-releasing action. These results suggest that at least part of the stimulatory action of the peptide on pituitary hormone release is brought about by prostaglandins. The failure of indomethacin to block the release of ACTH induced by cachectin suggests that other mechanisms may be involved in the release of ACTH induced by this peptide. Since the concentrations of cachectin required to stimulate pituitary hormone release are similar to those that are encountered in plasma during infection, it is likely that this direct pituitary action has pathophysiological significance.

Adrenocorticotropic Hormone↗

PubMed2004

Changes of hypothalamus-pituitary hormones in patients after total removal of craniopharyngiomas.

BACKGROUND: This paper aimed to elucidate the changes of hypothalamus-pituitary hormones in patients after total removal of craniopharyngiomas. METHODS: A total of 40 patients with craniopharyngiomas received surgery. The levels of triiodothyronine (T3), thyroxine (T4), thyrotropic hormone (TSH), antidiuretic hormone (ADH), and adrenocorticotropin (ACTH) were measured in the 40 patients before surgery and one week after surgery respectively. RESULTS: Twenty-eight patients (70%) had hypothyroidism before surgery, but 38 (95%) had hypothyroidism after surgery (P < 0.01). Twenty-three patients (57.5%) had diabetes insipidus (DI) before surgery and 38 (95%) had DI after surgery (P < 0.001). The pre- and post-operative levels of ADH were (2.49 +/- 0.30) pg/ml and (2.80 +/- 0.29) pg/ml respectively (P > 0.05), whereas those of ACTH were (23.97 +/- 2.69) pg/ml and (15.60 +/- 1.91) pg/ml respectively (P < 0.05). CONCLUSIONS: Hormone deficits after total removal of craniopharyngioma appear to be the common complication of surgery. Hypothyroidism and diabetes insipidus are more frequent after surgery than before surgery. Thyroxine and glucocorticoids should be administered routinely after total removal of craniopharyngioma.

Adolescent↗

PubMed2002

The effects of centrally administered apelin-13 on food intake, water intake and pituitary hormone release in rats.

Apelin is the recently identified endogenous ligand for the G-protein-coupled receptor, APJ. Preproapelin and APJ mRNA are found in hypothalamic regions known to be important in the regulation of food and water intake, and pituitary hormone release. The effects of intracerebroventricular (ICV) administration of pyroglutamylated apelin-13 on food and water intake and pituitary hormone release in rats were investigated. Apelin-13 had little effect on food intake, but dose-dependently increased drinking behaviour and water intake at 1 h. Apelin-13 (10 nmol) increased water intake by up to sixfold compared to saline. Compared to saline control, apelin-13 (10 nmol) significantly increased plasma ACTH and corticosterone and decreased plasma prolactin, LH and FSH at 30 min. In vitro, apelin-13 stimulated the release of CRH and AVP from hypothalamic explants, but had no effect on NPY release. These results suggest that apelin may play an important role in the hypothalamic regulation of water intake and endocrine axes.

Animals↗

PubMed1989

Hypothalamic action of cachectin to alter pituitary hormone release.

Cachectin (tumor necrosis factor, TNF) is a macrophage hormone which is released during infection and after injection of bacterial lipopolysaccharides. We have already demonstrated that the peptide has direct action on the pituitary to alter pituitary hormone release in vitro. To evaluate its action in vivo, we injected it into the third ventricle (3V) of conscious, male rats and measured its effect on various anterior pituitary hormones. The peptide produced an elevation in rectal temperature measurable on first measurement at 1 hour postinjection which was maintained for 3 hours. The maximal increase in body temperature was 1-1.5 degrees C and maximal effect was obtained by a dose as low as 1 ng (0.3 pmol) of the peptide. Preinjection of indomethacin into the 3V 1 hour prior to injection of TNF completely blocked the effect on body temperature without producing an alteration in rectal temperature itself which suggests that the elevation in body temperature may be mediated by prostaglandins. Following the intraventricular injection of various doses of TNF, there was no significant effect on plasma adrenocorticotropin (ACTH) except with the highest, 100 ng dose tested, which evoked a small but significant increase in plasma ACTH with a delay of 1 to 2 hours. Thus, the dose necessary to release ACTH was much higher than that required to elevate body temperature. The effect was no longer significant in indomethacin-pretreated animals suggesting a role for prostaglandins in the effect. This highest dose of intraventricularly administered TNF also produced a relatively modest, but significant, delayed increase in plasma GH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

The development of monoclonal antibodies against salmon (Oncorhynchus kisutch and O. keta) pituitary hormones and their immunohistochemical identification.

Monoclonal antibodies (MCAs) directed against several salmon pituitary hormones were generated by the fusion of myeloma cells with spleen cells from mice that had been immunized with either chum salmon (Oncorhynchus keta) growth hormone (GH) or prolactin (PRL), or one of two purified protein preparations from coho salmon (O. kisutch) pituitaries. Hybridoma were cloned by limiting dilution and screened for MCA production using immunohistochemical procedures. MCAs were generated that bound specifically to GH, PRL, or gonadotropic cells. MCAs were generated that bound to either fine granular material or large globular inclusions in the cytoplasm of the "classical" strongly PAS-positive globular gonadotropic cell type found in mature fish. This suggests that these MCAs are directed against gonadotropin II (GTH II). A MCA was also generated that bound both granular and globular material in the globular gonadotrops and granular material in the weakly PAS-positive vesicular gonadotrops in pituitaries from mature fish and to a cell type in immature rainbow trout pituitaries which is tentatively identified as the gonadotropin I (GTH I) cell type. This MCA did not bind to thyrotrops in immature rainbow trout pituitaries.

Animals↗

PubMed1983

Pituitary hormone release in response to food ingestion: evidence for neuroendocrine signals from gut to brain.

The synchrony of PRL and cortisol release with feeding is now well established. To delineate further the neuroendocrine mechanisms involved, meal-related pituitary and adrenal cortical activities were investigated in seven normal men in a series of experiments conducted in random sequence at 1-week intervals. Ingestion of a standardized mixed meal elicited a consistent acute release of PRL and cortisol at noon (1200 h), but not at breakfast (0800 h). No measurable changes in other pituitary hormones were observed. The relative magnitudes of PRL and cortisol release in response to lunch were not significantly influenced by a preceding breakfast. These responses appear unrelated to the cephalic or oral phases of food ingestion. However, the composition of the meals was found to be important. Whereas carbohydrate meals had no discernible effects, high protein meals induced a large increase in both PRL and cortisol; high fat meals caused selective release of PRL. Ingestion of L-tyrosine and L-tryptophan induced remarkable increments in serum concentrations of both PRL and cortisol, suggesting that these essential amino acids may be active components of the high protein meal. Choline had no effect. Meal-mediated PRL and cortisol release was unaffected by prior receptor blockade of the opioidergic and cholinergic systems with naloxone and atropine, respectively. These observations indicate that the protein component of the meal was responsible for the midday surges of PRL and cortisol and that the cephalic-vagal pathway was not required in food-entrained pituitary hormone release. Further, our data suggest that the neurotransmitter substrates in the protein meal may serve to link the gut and brain by modifying central catecholamine and serotonin biosynthesis, and thereby influence the hypothalamic factors controlling pituitary PRL and ACTH secretion. The possibility that gastrointestinal hormones may also influence the hypothalamic-pituitary system remains to be explored.

Adult↗

PubMed1992

Effects of thymosin alpha-1 on pituitary hormone release.

The thymosins are a family of hormone-like products of epithelial cells of the thymus which are important in maintenance and function of the immune system. Thymosin fraction 5, a partially purified extract of calf thymus, can influence pituitary hormone release. We have studied the effects of thymosin alpha 1 (T alpha 1), the first peptide isolated from thymosin fraction 5, on thyrotropin (TSH), adrenocorticotropin (ACTH), prolactin (Prl) and growth hormone (GH) release. To evaluate its effect in vivo we injected the peptide into the third ventricle of conscious male rats and measured the concentration of the pituitary hormones in plasma at different times after the injection. Following third-ventricular injection of T alpha 1, there was a significant decrease in plasma TSH and ACTH concentrations in comparison with values of control groups injected with diluent. The decrease in plasma TSH was of longer duration and was obtained with a lower dose of T alpha 1 than that of ACTH. Also, a significant decrease in plasma Prl was observed, with the same dose as for TSH. On the other hand, there were no significant changes in plasma GH. To examine if there is any direct effect of T alpha 1 at the pituitary level, we incubated hemipituitaries from male rats in vitro with different concentrations of the peptide. In this system T alpha 1 evoked a dose-dependent release of TSH and ACTH, while there was no effect on the release of Prl and GH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed2001

Pituitary hormone and insulin responses to infusion of amino acids and N-methyl-D,L-aspartate in horses.

Thirty-nine adult light horse mares, geldings, and stallions were used in two experiments to assess the pituitary hormone and insulin responses to infusions of arginine, aspartic acid, lysine, glutamic acid, and N-methyl-D,L-aspartate (NMA). In Exp. 1, 27 horses were assigned to one of three infusion treatments: 1) physiological saline (1 L); 2) 2.855 mmol of arginine/kg BW in 1 L of water; or 3) 2.855 mmol of aspartic acid/kg BW in 1 L of water. In Exp. 2, 12 horses were assigned, in a multiple-square 4 x 4 Latin square design, to one of four infusion treatments: 1) 2 mL of saline/kg BW; 2) 2.855 mmol of lysine/kg BW in water; 3) 2.855 mmol of glutamic acid/kg BW in water; or 4) 1 mg of NMA/kg BW in water. In Exp. 1, an acute (within 20 min) release of growth hormone (GH) was induced (P = 0.002) by aspartic acid. In contrast, acute release of prolactin (P = 0.001) and insulin (P = 0.002) was induced only by arginine; moreover, the arginine effect on insulin was present only in mares (P = 0.011). In Exp. 2, an acute release of GH was induced (P = 0.001) by glutamic acid and NMA. In males, the glutamic acid-induced GH release was greater than that of NMA; in mares, the NMA-induced GH release was greater than that of glutamic acid (P = 0.069). Both lysine and glutamic acid induced (P = 0.001) acute release of prolactin, whereas an acute release of insulin was elicited (P = 0.002) only by lysine. The NMA-induced LH response was due almost entirely to the response in mares and stallions (P = 0.016), and the NMA-induced FSH release was due almost entirely to the response in mares (reproductive status effect; P = 0.004). In the horse, aspartic acid, glutamic acid, and NMA seem to stimulate GH release; arginine and lysine seem to stimulate prolactin and insulin release; and NMA seems to stimulate LH and FSH release. It seems that N-methyl-D-aspartate glutamate receptors are involved in controlling GH, LH, and FSH secretion, whereas other mechanisms are involved with prolactin secretion. These results also indicate that gonadal steroids interact with amino acid-induced pituitary hormone release in adult horses.

Amino Acids↗

PubMed2003

Expression of pituitary hormones in the Pax8-/- mouse model of congenital hypothyroidism.

Signaling mechanisms in pituitary morphogenesis as well as pituitary cell fate determination during early embryonic development are relatively well characterized. In contrast, the cues that determine the progression of the various anterior pituitary cell types during postnatal periods are poorly defined. Pax8-/- mice, which are born without a thyroid gland, were used to study the influence of thyroid hormones on the expression of pituitary hormones during early postnatal life. Serum pituitary hormones were determined by RIAs, and the pituitaries were analyzed by Northern blotting, in situ hybridization histochemistry, and immunocytochemistry. In 21-d-old Pax8-/- mice, the cellular composition of the anterior pituitary was dramatically distorted. Thyrotropes exhibited hypertrophy and hyperplasia, the number of detectable somatotropes was drastically reduced, and lactotropes were almost undetectable. Expression of LH and FSH was also reduced, but ACTH and proopiomelanocortin expression was not significantly different. Serum pituitary hormone levels were changed correspondingly. T(4) replacement therapy for variable time periods normalized TSH and GH mRNA expression within 3 d but not prolactin expression, not even when T(4) was administered for 6 d in combination with estradiol. These findings reveal the importance of thyroid hormones in developing the appropriate proportions of anterior pituitary cell types, especially with regard to lactotropes.

Age Factors↗

PubMed2004

Pituitary hormone deficiencies due to transcription factor gene alterations.

Mechanisms that control pituitary development are gradually better understood. They involve molecular signals from surrounding structures and the expression of a cascade of homeodomain transcription factors. Mutations of these transcription factors cause defects of embryologic development of the anterior pituitary responsible for isolated or multiple pituitary hormone deficiencies (respectively, IPHD and MPHD) in both rodents and humans. In this review we emphasize the description of human phenotypes associated with genetic alterations found in IPHD (e.g. isolated corticotroph deficiency and Tpit mutations) and MPHD (mutations of POU1F1, PROP1, Hesx1, Lhx3, Lhx4, Ptx2).

Cell Differentiation↗

PubMed1985

The effect of lisuride hydrogen maleate on anterior pituitary hormones, oestradiol and cortisol in normal and hyperprolactinaemic women.

The effects of single oral doses of 0.1 mg lisuride hydrogen maleate (lisuride), a semisynthetic ergot derivative given at 09.00 h, on the serum levels of prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), thyroid-stimulating hormone (TSH), oestradiol and cortisol were studied in six normally cycling women and six patients with hyperprolactinaemic amenorrhoea. The same subjects received placebo and the results were compared with those of lisuride. Within 1 h after oral administration of lisuride, PRL levels decreased significantly (P less than 0.05) and reached the lowest level at 4 h after ingestion and stayed low until 8 h in both normal women and hyperprolactinaemic patients. LH levels slightly but not significantly decreased after lisuride administration in hyperprolactinaemic patients. Serum cortisol levels increased at 13.00 h, probably due to the effect of meal. No significant differences between the lisuride group and placebo group were observed in GH, TSH, FSH and oestradiol levels. These results suggest that lisuride acts as a long-acting prolactin suppressor and that it has little effects on the secretion of other pituitary hormones. Therefore, this drug could be useful for treatment of hyperprolactinaemic patients.

Adult↗

PubMed1961