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At least 937 records · Page 52Linked to original sources
PubMed2002

Effects of vasoconstriction on the acute anterior pituitary hormonal response to head injury.

Since cerebral vasoconstriction alone may impair the hypothalamic and pituitary circulation, we planned to investigate whether the hormonal response to the vasoconstriction that may be induced by the head injury is a significant component of the general acute hormonal response to head injury. Although diffuse adrenocorticotropic hormone immunohistochemical staining of the adenohypophysis of rabbits was observed in the head trauma administered group, only mild positive staining was present in the Endothelin-1 administered group. However, decreased prolactin staining was found in both of the groups. It is postulated that trauma induced vasoconstriction may not be an important manipulating factor in the corticotrophic hormone response to injury, while it may be responsible for the decreased prolactin response.

Adrenocorticotropic Hormone↗
PubMed1994

Assessment of the labeling index of cohorts of the anterior pituitary cell population in phenobarbital-treated male rats by a double immunohistochemical technique for bromodeoxyuridine and pituitary hormones.

A previous study demonstrated that administration of phenobarbital for up to 7 days to male AP Wistar rats caused alterations in labeling indices (LIs) of several different tissues as determined by immunohistochemical visualization of bromodeoxyuridine (BrdU) incorporation into S-phase nuclei. The pivotal role of the pituitary gland in the function of the endocrine system and changes in circulating hormone levels that result from administration of xenobiotics prompted our consideration of the possible changes in LIs of individual cohorts of the anterior pituitary cell population that may occur as a specific functional adaptation during phenobarbital administration. We evaluated the LIs of individual anterior pituitary cell cohorts by modifying a double immunohistochemical staining method for bromodeoxyuridine and pituitary hormones using a sequential peroxidase-anti-peroxidase (PAP)/alkaline phosphatase-anti-alkaline phosphatase (APAAP) method employing diaminobenzidine and New Fuchsin chromogens, respectively. The method was robust and reproducible. Differences were noted in individual anterior pituitary cohort LIs between control and phenobarbital-treated groups, although no statistically significant difference was evident. We conclude that no detectable effects on individual cohort LIs were induced by treatment with phenobarbital for up to 7 days and that any functional adaptation to treatment was associated with increased hormone release. We believe that the visualization, identification, and quantitation of replicating cells in specific hormone-positive cohorts of the anterior pituitary cell population provide opportunities for understanding the influence of xenobiotics and disease processes on pituitary function.

Animals↗
PubMed1994

Alteration of basal release of anterior pituitary hormones by pretreatment of primary cultured cells with trypsin.

The anterior pituitary (AP) gland secretes 6 different hormones. Prolactin (PRL) is secreted at a relatively high level without stimulation by the hypothalamus, while secretion of the others requires the action of stimulatory factors from the hypothalamus. In order to gain an insight into the mechanism underlying the different spontaneous release patterns of these hormones, we investigated their spontaneous release rate after pretreating rat anterior pituitary cells with trypsin. Rat AP cells were cultured on Cytodex microcarrier beads for 4 days and were then superfused with either control medium or medium containing trypsin (0.25%) for 5 min. The subsequent release rates of the AP hormones were monitored. The basal release of PRL was severely reduced to almost undetectable level and began to recover 120 min after the trypsin-pretreatment. Full recovery was attained over the next 100 min and was delayed by treatment with a protein synthesis inhibitor, cycloheximide (7 microM). In the trypsin-pretreated cells, basal release of PRL and growth hormone (GH) was severely reduced, while that of thyroid stimulating hormone (TSH) and adrenocorticotropic hormone (ACTH) was enhanced and luteinizing hormone (LH) and follicle stimulating hormone (FSH) was not markedly affected by the treatment, suggesting that the suppression of PRL release was not caused by nonspecific damage to the cells. Since trypsin does not readily enter cells, the altered secretion of AP hormones seems to be the result of restricted digestion of the external components of the cells. On the bases of these observations, we predicted that the mechanism of spontaneous release of hormones involves trypsin sensitive proteins (TSMP) on the plasma membranes of the anterior pituitary cells.

Animals↗
PubMed1983

Pituitary hormones and contact sensitivity in rats.

Hypophysectomized (Hypo-X) rats do not develop contact sensitivity to dinitrochlorobenzene (DNCB). Daily treatment with prolactin or growth hormone completely restores the DNCB-reactivity of Hypo-X animals. Treatment of such animals with ACTH, FSH, LH, TSH or HCG has no restoring potential. Treatment with ACTH in addition to prolactin or growth hormone antagonizes restoration of Hypo-X rats. These experiments indicate that the pituitary gland has the potential of regulating contact sensitivity.

Adrenocorticotropic Hormone↗
PubMed1998

Autosomal recessive deficiency of combined pituitary hormones (except ACTH) in a consanguineous Brazilian kindred.

Familial hypopituitarism represents a clinically and genetically heterogeneous disorder. In a subset of these families, defects in Pit-I, a transcription factor essential for proper pituitary development have been identified as underlying molecular cause. These patients present extreme short stature, GH, PRL and TSH deficiency but intact ACTH, LH and FSH secretion. The pituitary is usually hypoplastic. In this report we describe a consanguineous family (the parents are first cousins) with thirteen siblings. Of the ten living siblings, four (two males and two females) have panhypopituitarism with severe growth failure. They had evidence of growth hormone, prolactin and gonadotropin deficiencies and developed central hypothyroidism late in life. ACTH secretion was normal. Bone age was retarded and dual-photon bone densitometry indicated severe osteoporosis. Combined provocative tests for pituitary hormones indicated blunted responses for GH, LH, FSH and a modest rise in serum PRL and TSH. A clonidine-test failed to induce pituitary GH response. A corticotropin-releasing factor (CRF) provocative test was conducted after 6 months without the use of prednisone with a normal ACTH response after CRF in the affected sibling. Plasma IGF-I and IGF-BP3 were below normal levels. Serum E2 (females) and serum testosterone (males) levels were very low. MRI evaluation of the pituitary indicated pituitary aplasia in all subjects. The phenotype described in this kindred is different from families reported with Pit-1 mutations. However, it resembles previously published kindreds with similar clinical and biochemical findings. The relative preservation of ACTH suggests a genetic defect early in pituitary gland development.

Adolescent↗
PubMed1975

Pituitary hormonal reserve in patients presenting hyperprolactinemia, intrasellar masses, and amenorrhea without galactorrhea.

The pituitary release of gonadotropins, prolactin, and TSH after the simultaneous intravenous administration of 50 mug LH-RH was 400 mug TRH was evaluated in 7 amenorrheic women with sellar enlargement and hyperprolactinemia. It was found that only minimal amounts of LH and FSH were released by LH-RH. All patients had elevated serum prolactin levels but TRH administration elicited negligible release of prolactin. This was in contrast to the normal TSH response to TRH in most of these women. It is concluded that intrasellar masses may be associated with hyperprolactinemia which does not necessarily cause galactorrhea and that impaired gonadotropin reserve correlates with the presence of amenorrhea.

Adult↗
PubMed1980

[Morphological identification of pituitary hormones by the aid of pH-determination using microphotometry (author's transl)].

The identification of pituitary ACTH and TSH producing cells was performed by histological staining at the isoelectric points (pH levels: 4.6 and 5.2 respectively) of these hormones in cat. Intensity of stained material in the hormone producing cells was determined by microphotometric technique. By the application of hormones influencing the pituitary ACTH and TSH producing relevant changes in pituitary cells could be detected.

Adrenalectomy↗
PubMed1986

Satellite cell proliferation in response to pituitary hormones.

Proliferation of rat skeletal muscle satellite cells was studied in vitro, and their ability to respond to a variety of protein hormones was examined, including: growth hormone, prolactin, luteinizing hormone, thyrotropin and fibroblast growth factor. All experiments were conducted in serum-free medium to avoid complicating interactions with serum constituents such as other hormones or binding proteins. Dose-response curves were constructed for each protein and encompassed the physiological range plus concentrations two to three orders of magnitude greater than the physiological range. Of the proteins examined, the only one shown to have the ability to directly stimulate satellite cell proliferation was fibroblast growth factor. None of the anterior pituitary protein hormones had the ability to interact directly with satellite cells to stimulate proliferation in vitro. Therefore, satellite cells seem to be selective in their response to protein hormones, and the classes identified thus far are hormones in the insulin-like growth factor family and fibroblast growth factor. These two classes of protein hormones are quite different and would not be expected to act through a common pathway. Consequently, we have proposed a dual regulatory system that may allow for local as well as systemic stimulation of satellite cells.

Animals↗