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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a preliminary report we described the effects of rat prolactin on the incorporation of [14C]acetate into lipids by a cell line from a dimethylbenz(a)anthracene-induced rat mammary tumor. The characteristics of the response to prolactin were very similar to those described for the normal rat mammary gland; namely, insulin was required for full expression of the response, maximal activity was not seen until 36 hr after the addition of the hormones, and growth hormone was able to elicit the same response. However, we were unable to detect binding of 125I-labeled prolactin to these cells, and furthermore, other more purified prolactin preparations were inactive. Upon further investigation we discovered that the activity resided in a low-molecular-weight fraction of the rat prolactin B-1 preparation and was probably either vasopressin or oxytocin or both. These data suggest the possibility that vasopressin may play a role in rodent mammary tumorigenesis.
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PMID:Vasopressin stimulation of acetate incorporation into lipids in a dimethylbenz(a)anthracene-induced rat mammary tumor cell line. 10 Feb 17

Lactation is controlled by hormones from several endocrine glands. An undisturbed function of the anterior pituitary, of the adrenals, and of the ovaries is a prerequisite for a normal morphogenesis of the mammary gland. The epithelial ducts proliferative under the combined influence of estrogens, glucocorticoids and growth hormone, whereas the lobuloalveolar development depends on progesterone and prolactin in addition to the fore-mentioned hormones. During pregnancy pituitary prolactin may be substituted by placental lactogen. Milk synthesis begins in the second half of pregnancy. It is supported by prolactin and cortisol, which directly act on enzyme activities and processes of differentiation of the alveolar cells. The sudden surge in the secretion of milk after parturition is most likely due to the rapid decline of the serum levels of progesterone. The ejection of milk from the lactating mammary gland is controlled by a neuroendocrine reflex mechanism. Suckling is the appropriate stimulus for the release of oxytocin from the posterior pituitary. Oxytocin increases intramammary pressure by inducing contraction of the myoepithelial cells and thus aids in expelling the milk from the mammary glands. Maintenance of normal postpartum lactation depends on frequent and intensive suckling. Suckling does not only stimulate the release of oxytocin, but also provokes secretion of prolactin and ACTH. This increase in prolactin caused by suckling guarantees galactopoesis. Influencing secretion of prolactin has been proven to be a useful tool for regulating lactation. The experimental ergot derivative 2-Brom-alpha-ergocryptine is a potent suppressor of prolactin secretion from the anterior pituitary. In contrast to estrogens, alone or in combination with progestagens or androgens, this drug is not only effective in suppressing the onset of lactation, but also in inhibiting lactation once milk secretion had started. As to stimulating lactation in the human there is no effective drug available up to now.
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PMID:[Hormonal regulation of lactation (author's transl)]. 18 42

The stimulating effect of different pituitary hormones on longitudinal bone growth was determined with tetracycline as intravital marker in hypophysectomized rats. Growth hormone was found to be the most effective growth stimulating pituitary hormone. At considerably higher doses, thyrotrophic hormone (TSH) and prolactin also showed growth stimulating pituitary hormone. At considerably higher doses, thyrotrophic hormone (TSH) and prolactin also showed growth stimulating activity. TSH exerts its effect via the production of thyroxine, whereas the growth stimulation by prolactin seems to be a direct effect of this hormone, similar to the effect of growth hormone. The LH, FSH, ACTH, MSH, vasopressin and oxytocin preparations did not stimulate longitudinal bone growth.
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PMID:Stimulation of longitudinal bone growth by hypophyseal hormones in the hypophysectomized rat. 19 Aug 39

Prolactin, as a "broad spectrum hormone", has been described to exert also vascular and renal actions in laboratory animals and in humans. However, prolactin preparations of various species are contaminated with neurohypophysial hormones (ADH, oxytocin) which possess vascular and renal activities. Antisera against ADH, oxytocin and prolactin are rather specific inactivators of the biologic activity of the respective hormone; the oxytocinasevasopressinase system of pregnancy plasma destroys ADH and oxytocin. Incubation-identification procedures with antisera against ADH, oxytocin and prolactin and with pregnancy plasma revealed that changes in blood pressure, urine flow and urinary osmolarity cannot be ascribed to prolactin per se but to the ADH impurity of prolactin preparations. Furthermore, recent metabolic studies in normally hydrated, overhydrate and dehydrated animals and humans have shown that prolactin does not affect renal water and electrolyte excretion. Thus, earlier reports on vascular and renal activity of prolactin in laboratory animals and humans should be viewed with great caution. Elimination of neurohypophysial hormone impurities of prolactin preparations by incubation with either ADH and oxytocin antisera or with pregnancy plasma provides techniques for better assessment of the real biologic effects of the prolactin molecule.
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PMID:Renal and vascular activity of prolactin preparations. Contamination of prolactin preparations with ADH and implications on renal and vascular prolactin research. 43 76

We have analyzed the plasminogen activator (PA) content of normal rodent mammary glands at different stages of the mammary life cycle and after exposing the animals to various hormones; we have also assessed the PA response of mammary explants to a variety of hormonal environments. Similar studies were performed on a limited number of primary mammary tumors. Plasminogen activator production was clearly correlated with mammary involution. A large but transient increase in enzyme content followed the initiation of involution in all glands, and the enzyme was produced by mammary cells, not by macrophages or granulocytes. Oxytocin, prolactin and hydrocortisone, which slowed or blocked involution, produced parallel effects on gland regression and PA synthesis. PA synthesis by explants in organ culture was induced by hormonal environments that fostered involution and repressed by those that promoted lactation. Mammary tumors produced much more PA than normal tissue both in vivo and in vitro, and distinct differences were found in the response of enzyme synthesis to hormones. The results reinforce the association of PA with tissue remodeling; show that the enzyme can be used as an indicator of cellular response to a wide range of hormones in both normal and malignant tissue; and suggest that observations of this type in organ culture may be of some value in predicting physiological responses in vivo.
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PMID:Mammary plasminogen activator: correlation with involution, hormonal modulation and comparison between normal and neoplastic tissue. 45 56

Estradiol, progesterone, prolactin, and 13,14-dihydro-15-keto prostaglandin F2alpha (PGFM) were measured in both maternal and cord venous blood obtained at the time of delivery in 24 maternal infant pairs evenly divided among six different physiologic groups. Progesterone and prolactin were significantly higher and estradiol was significantly lower in cord than in maternal blood. There were no significant differences between the groups for cortisol, estradiol, or progesterone in maternal or cord blood. A significant increase in prolactin was demonstrated in women receiving oxytocin for induction of labor. Both estradiol and PGFM were highly correlated between maternal and cord blood. PGFM was significantly higher in cesarean section patients in labor than in those not in labor in both the maternal and cord circulations. Among those delivered vaginally, PGFM tended to be higher in those in spontaneous labor than in those with induced labor. PGFM in induced labor was intermediate between spontaneous labor aptients delivered by cesarean section and those delivered vaginally. Duration of labor was negatively correlated with cord estradiol concentration. The physiologic significance of these findings is discussed.
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PMID:Interrelationships between maternal and cord prolactin, progesterone, estradiol, 13,14-dihydro-15-keto-prostaglandin F2alpha, and cord cortisol at delivery with respect to initiation of parturition. 56 75

Since impurities consisting of neurohypophysical hormones in prolactin powder may be responsible for the vascular and renal effects attributed to prolactin, rat (NIH-RP-1), ovine (NIH-P-S-10, S-12), and bovine (NIH-P-B4) prolactin preparations were examined for their content of ADH and oxytocin by rat antidiuresis, milk-ejection, and blood pressure assays. Activities were identified as due to ADH or oxytocin by incubation of prolactin solutions with antisera against ADH, oxytocin, and prolactin, or with pregnancy plasma. The ADH content of rat, ovine (P-S-10, P-S-12) and bovine prolactin was found to be 104.5 +/- 7.1 (means +/- SE), 2.5 +/- 0.2, 1.6 +/- 0.1, and 1.6 +/- 0.5 mU/mg powder, respectively; the corresponding values for oxytocin content were 155.3 +/- 3.5, 1.2 +/- 0.1, 0.5 +/- 0.1, and 1.2 +/- 0.01 mU/mg powder, respectively. Because antidiuretic, milk-ejection, and blood pressure activities of the various prolactins were eliminated after incubation with antisera against ADH and oxytocin, or with pregnancy plasma, but not with prolactin antisera, it is concluded that the reported vascular and renal prolactin effects are attributable to ADH contamination of the prolactin preparation rather than to the prolactin molecule itself. These findings have implications for renal and vascular prolactin research.
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PMID:Contamination of prolactin preparations by antidiuretic hormone and oxytocin. 56 96

The effects of changes in the intensity of the suckling stimulus on the reflex release of oxytocin and prolactin were compared in urethane-anaesthetized lactating rats. Mothers which had previously suckled 12 pups (Group 1) showed a graded increase in the amount of oxytocin released during a 3 h suckling test when the number of pups applied to the nipples was increased from six to eight or ten. Mothers which had suckled six pups during their lactation (Group 2) appeared to show a maximum frequency of milk ejection whether six, eight or ten pups were applied to the nipples. The release of prolactin was not elicited from either Group 1 or Group 2 mothers when six pups were applied to their nipples. With eight pups suckling, the Group 1 mothers again showed no evidence of prolactin release. In contrast, the Group 2 mothers showed a significant increase in the level of prolactin in the plasma during the 3 h suckling test. With ten pups suckling the release of prolactin was evident in both groups of mothers, although the response was earlier and more pronounced in Group 2 than Group 1. These results suggest that in the urethane-anaesthetized rat, the threshold for the suckling-induced reflex release of oxytocin is distinct from the threshold for the release of prolactin and that these thresholds are, at least in part, set by the preceding suckling experience of the mothers. In those animals which showed both reflex milk ejection and prolactin release there was a linear relationship between the magnitude of the two endocrine responses.
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PMID:Relationship between the suckling-induced release of oxytocin and prolactin in the urethane-anaesthetized lactating rat. 63 21

A significant elevation in plasma prolactin was observed 10 min following the intravenous injection of 100 microgram of melatonin into either estrogen-progesterone (EP) primed or into nonsteroid-treated male rats. 60 min postinjection in the EP primed rat, the groups treated with 100 microgram or 10 mg of melatonin had signficantly elevated plasma prolactin levels while no effect was observed with these same doses in the nonsteroid-treated rats. Compared to diluent-treated controls, a significant elevation in plasma prolactin was observed at 10, 20 and 60 min following the intravenous injection of either 1 microgram arginine vasotocin (AVT) or 1 mg melatonin into EP primed male rats. A consistent rise in plasma prolactin was also evident after the injection of 1 microgram of either arginine vasopressin, lysine vasopressin or AVT. Oxytocin had no effect on plasma prolactin values. The intravenous administration of 1 microgram of (deamino-1,6 dicarba, 8-arginine)-vasotocin caused a significant elevation of plasma prolactin 10 and 20 min after injection. However, the injection of another analogue of AVT, (4-leucine, 8-arginine)-vasotocin, had no effect on prolactin release at the time points measured.
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PMID:Effects of melatonin and natural and synthetic analogues of arginine vasotocin on plasma prolactin levels in adult male rats. 66 73

Lesions of the median raphe (MR) nucleus were placed in cycling female rats and their ability to lactate was evaluated following subsequent pregnancies. Pups from MR-lesioned (MRL) animals grew more slowly and had greatly impaired survival rates compared to pups from sham-lesioned animals. Chronic treatment of MRL mothers with oxytocin (Oxy; 1 IU, s.c., once or twice/day) did not increase the growth rates of their litters. Acute responses to exogenous Oxy (1 IU, i.p.) in MRL mothers, measured by the weight gain of litters during 1/2-h suckling intervals before and after injection, were marginally significant. Milk yield during the total hour suckling period (stomach contents of pups) was clearly less in the MRL animals (p less than 0.01). Treatment with either prolactin (Prl; 250 microgram, twice/day), Prl + GTC (4 mg/kg gorwth hormore, 30 microgram/kg thyroxine, 0.5 mg/rat cortisol, once/day), or 5-HTP (75 mg 5-hydroxytryptophan/kg, twice/day) did not improve the growth rates of litters from MRL animals. However, when milk yield (stomach contents after 1 h) following a 14-h non-suckling interval was measured, lactogenic hormones (Prl or Prl + GTC) restored milk yield in MRL animals to control levels. This response was clearly not dependent upon exogenous Oxy. These results suggest that deficits in the release of lactogenic hormones are involved in the impairments in lactation following lesions of the MR nucleus.
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PMID:Impairments in lactation in the rat following destruction of the median raphe nucleus. 69 8


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