INFLUENCE OF HORMONES ON LOBULO-ALVEOLAR DIFFERENTIATION OF MOUSE MAMMARY GLANDS IN VITRO

1966 ◽  
Vol 35 (4) ◽  
pp. 331-NP ◽  
Author(s):  
RUBY R. ICHINOSE ◽  
S. NANDI

SUMMARY (1) To induce mammary differentiation in vitro, BALB/cCrgl mice were given hormones before incubation of their mammary glands in defined medium containing steroid hormones (oestradiol, progesterone and aldosterone), anterior pituitary hormones (prolactin and growth hormone), and insulin. The sequence of lobule development in vitro obtained in this way was determined by cultivation of tissues for 1, 2, 3, 4 and 5 days. Lobules appeared on the 3rd day of culture, although proliferation occurred throughout the 5-day period. (2) In two other sets of experiments, mammary glands were exposed to various combinations of hormones in culture. Survival of cultured tissues required the presence of insulin, whereas differentiation required the presence of steroid hormones, anterior pituitary hormones, and insulin. Of the steroid hormones used, aldosterone alone fulfilled the minimum steroid hormone requirement for lobule formation in vitro.

1993 ◽  
Vol 129 (6) ◽  
pp. 489-496 ◽  
Author(s):  
Andreas Kjær

Secretion of the anterior pituitary hormones adrenocorticotropin (ACTH), β-endorphin and prolactin (PRL) is complex and involves a variety of factors. This review focuses on the involvement of arginine-vasopressin (AVP) in neuroendocrine regulation of these anterior pituitary hormones with special reference to receptor involvement, mode of action and origin of AVP. Arginine-vasopressin may act via at least two types of receptors: V1− and V2−receptors, where the pituitary V1−receptor is designated V1b. The mode of action of AVP may be mediating, i.e. anterior pituitary hormone secretion is transmitted via release of AVP, or the mode of action may be permissive, i.e. the presence of AVP at a low and constant level is required for anterior pituitary hormones to be stimulated. Under in vivo conditions, the AVP-induced release of ACTH and β-endorphin is mainly mediated via activation of hypothalamic V1− receptors, which subsequently leads to the release of corticotropin-releasing hormone. Under in vitro conditions, the AVP-stimulated release of ACTH and β-endorphin is mediated via pituitary V1b− receptors. The mode of action of AVP in the ACTH and β-endorphin response to stress and to histamine, which is involved in stress-induced secretion of anterior pituitary hormones, is mediating (utilizing V1− receptors) as well as permissive (utilizing mainly V1− but also V2−receptors). The AVP-induced release of PRL under in vivo conditions is conveyed mainly via activation of V1−receptors but V2−receptors and probably additional receptor(s) may also play a role. In stress- and histamine induced PRL secretion the role of AVP is both mediating (utilizing V1 −receptors) and permissive (utilizing both V1− and V2− receptors). Arginine-vasopressin may be a candidate for the PRL-releasing factor recently identified in the posterior pituitary gland. Arginine-vasopressin of both magno- and parvocellular origin may be involved in the regulation of anterior pituitary hormone secretion and may reach the corticotrophs and the lactotrophs via three main routes: the peripheral circulation, the long pituitary portal vessels or the short pituitary portal vessels.


1978 ◽  
Vol 88 (2) ◽  
pp. 239-249 ◽  
Author(s):  
Loren G. Lipson ◽  
Inese Z. Beitins ◽  
Paul D. Kornblith ◽  
Janet W. Mc Arthur ◽  
Henry G. Friesen ◽  
...  

ABSTRACT A tissue culture study was undertaken to determine if human non-functioning pituitary tumours secrete polypeptide anterior pituitary hormones in vitro and to study the spectrum of hormone release by functioning pituitary neoplasms. Fragments from 48 human pituitary tumours (from patients - 2 with Cushing's disease, 1 with Nelson's syndrome, 5 with amenorrhoea-galactorrhoea, 10 with acromegaly and 30 with non-functioning pituitary tumours) and three normal human anterior pituitary glands (controls) were placed in tissue culture immediately after surgery. The in vitro release of human growth hormone (HGH), prolactin (Prl), thyrotrophin (TSH), adrenocorticotrophin (ACTH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) were measured by radioimmunoassays at the end of one week in culture. Clinical and pathological data were compared to hormone release patterns. In the culture media from control pituitaries the concentrations of the six hormones tested were 100 to 10 000 times greater than in peripheral blood. The medium surrounding the fragments from functioning pituitary tumours contained the following: a) Acromegaly - high levels of HGH and variable concentrations of the other hormones. b) Cushing's disease - ACTH and Prl predominantly. c) Amenorrhcea-galactorrhoea syndrome - prolactin in 4 out of 5 patients, all six polypeptides in one patient. In the media from the 30 patients diagnosed as having non-functioning pituitary tumours, 60 % of the samples contained at least one hormone at a concentration similar to that of the controls and 100 % of the samples contained detectable quantities of at least one hormone.


1968 ◽  
Vol 40 (1) ◽  
pp. 73-80 ◽  
Author(s):  
PATRICIA W. MAJOR ◽  
D. T. ARMSTRONG

SUMMARY Small doses of luteinizing hormone (LH) have been shown to exert a stimulating effect on the in vitro carbohydrate metabolism of the prepubertal rat ovary. In order to determine the specificity of the response, studies were undertaken comparing the effects caused by LH with those of other anterior pituitary hormones. Preparations of thyroid stimulating hormone (TSH) caused responses similar to those caused by LH, when added to the media in which prepubertal rat ovaries were incubated. A detailed study of the effects of TSH preparations (prepared by different procedures with known low levels of LH contamination) on lactic acid production, has been undertaken. All TSH preparations tested caused considerably greater stimulation of glycolysis than could be accounted for on the basis of their contamination with LH when the latter was appraised by the ovarian ascorbic acid depletion assay.


1961 ◽  
Vol 236 (4) ◽  
pp. 1002-1005
Author(s):  
Arnold N. Weinberg ◽  
Ira Pastan ◽  
Hibbard E. Williams ◽  
James B. Field

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