Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Synthetic human parathyroid hormone-related peptide (hPTHrP)-(1-34) fragment was compared with parathyroid hormone (bovine sequence, 1-34; bPTH-(1-34) for inhibiting oxytocin or prostaglandin F2 alpha (PGF2 alpha)-induced contractions on rat uterus in vitro. bPTH exhibited a potent (ED50 = 7 x 10(-9) M) inhibition on oxytocin-induced contractions. Both bPTH-(1-34) and hPTHrP-(1-34) were devoided of any significant effect upon PGF2 alpha-induced uterine contractions. Human PTHrP also inhibited oxytocin-induced uterine contractions (ED50 = 77 x 10(-9) M) and this effect, like that of bPTH, was dose dependent. Human PTHrP-(140-173) fragment had no significant effect on oxytocin-induced uterine contractions. The inhibitory effect of hPTHrP-(1-34) disappeared after pretreatment with [Tyr]34-bPTH-(7-34)-NH2, a competitive reversible antagonist of bPTH-(1-34). Thus PTHrP might be involved in the control of myometrial activity.
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PMID:Parathyroid hormone-related peptide inhibits oxytocin-induced rat uterine contractions in vitro. 138 75

Earlier studies have shown that lactation-induced bone loss in the rat is both PTH- and vitamin D-independent and have suggested the involvement of another, as yet unidentified, factor(s) in the altered calcium metabolism which accompanies lactation. In the present study, we investigated the possibility that PTH-related protein (PTHrP), which is produced in lactating mammary glands, is a putative calciotropic factor acting systemically during lactation. To test this hypothesis, we examined changes in urinary phosphate and cAMP excretion in relation to suckling since phosphaturia (P-uria) and increased urinary cAMP excretion are sensitive parameters of PTHrP action on the kidney. When lactating rats (separated from their pups overnight) were allowed to suckle pups for 1 h, they showed a marked P-uria which lasted 3-4 h. In most instances, a transient increase in cAMP excretion preceded the P-uria. These effects were not abolished by thyroparathyroidectomy; hence they are not attributable to a transient increase in PTH secretion. Administration of PRL or oxytocin did not induce significant P-uria. When lactating rats were pretreated with anti-PTHrP anti-serum, the suckling-associated P-uria was prolonged and augmented. This prolongation of P-uria was similar to the effects observed when exogenous PTHrP (1-34)amide was administered in the presence of the antiserum. These data support the hypothesis that some of the PTHrP produced in lactating mammary glands may be released systemically during suckling and act in an endocrine manner on target organs such as the kidney.
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PMID:Suckling-mediated increases in urinary phosphate and 3',5'-cyclic adenosine monophosphate excretion in lactating rats: possible systemic effects of parathyroid hormone-related protein. 165 80

Forskolin (FSK; an activator of adenylyl cyclase) and cortisol synergistically increase the concentration of oxytocin receptors (OTRs) in rabbit amnion cells. The aims of this study were to characterize potential physiological regulators of OTR concentrations acting through adenylyl cyclase and to clarify the mechanisms of potentiation by cAMP and cortisol. Both isoproterenol (ISO) and parathyroid hormone-related protein (PTHrP) elevated amnion cell cAMP levels and OTR concentrations. The effects of ISO and PTHrP on OTR were potentiated by cortisol. Cortisol had no effect on the ability of ISO or PTHrP to stimulate adenylyl cyclase activity, and cAMP did not affect the number or affinity of glucocorticoid receptors in whole cells or in cytosol. Adenylyl cyclase activation, however, caused conversion of mifepristone (RU486) from a glucocorticoid antagonist to agonist. Thus, mifepristone elevated OTR receptor concentrations in the presence of FSK. In contrast, a structurally related glucocorticoid antagonist, onapristone (ZK98 299), was unaffected by cAMP. Because glucocorticoid receptors bound to mifepristone are capable of interacting with DNA, whereas onapristone-occupied receptors are not, we conclude that cAMP affects glucocoticoid receptor-DNA interactions, accounting for the synergistic effects of cAMP and cortisol on OTRs.
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PMID:Effectors of cyclic adenosine 5'-monophosphate up-regulating-oxytocin receptors in rabbit amnion cells: isoproterenol, parathyroid hormone-related protein, and potentiation by cortisol. 852 7

Although milk yield of cows and goats is known to be closely related to the total flow of blood through the udder, a number of studies suggest that milk yield can vary independently. No studies have attempted to measure the proportion of total flow that is nutritive. Within the mammary gland, capillary networks form a basket-like architecture surrounding each alveolus. Notably, flow in individual capillaries is not constant and varies among capillaries. Capillary flow (measured by intravital microscopy) was decreased by oxytocin, which generally increased total flow in the mammary artery, suggesting that the proportion of total flow that is nutritive can vary. In addition to classic metabolic regulators (e.g., carbon dioxide and oxygen) of tissue blood flow, the mammary gland produces a number of vasodilatory compounds, including parathyroid hormone-related protein, insulin-like growth factor-I, prostacyclin, nitric oxide, and endothelin. All of these compounds have been shown to alter mammary blood flow. Mammary tissue also contains kallikrein and angiotensin-converting enzyme, which convert circulating kinins and angiotensin, respectively, into potent vasoactive compounds. A number of these compounds are produced by epithelial cells themselves, providing a mechanism for the functioning epithelium to control its own blood supply and, hence, nutrient flow for milk synthesis. In this review, we examine the nature of the mammary microcirculation, its behavior under different conditions, and some of the regulatory features of the mammary microvasculature.
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PMID:Regulation of blood flow in the mammary microvasculature. 887 13

A system for the study of the regulation of the release of triacylglycerols by mammary gland slices was developed. By prelabelling the triacylglycerol pool with [3H]oleate measurements of release of both mass of triacylglycerol and of newly synthesized triacylglycerol have been made. Oxytocin and ovine prolactin stimulated release of triacylglycerol and protein, but the former was 40-fold more effective. Recombinant bovine prolactin was even less active than ovine prolactin, suggesting that contamination of the latter with oxytocin and/or vasopressin was partly responsible for its stimulatory effect on release. The findings support the view that the major effect of oxytocin is to stimulate contraction of myoepithelial cells and thus release secreted lipid stored in the lumen of the mammary gland alveoli. Ionomycin, a Ca2+ ionophore, also stimulated lipid release, but probably not by the usual apocrine route. Parathyroid hormone-related protein, a peptide produced by the mammary gland, did not stimulate release or antagonize the effects of oxytocin. Release of lipid was also measured in mammary gland slices from late-pregnant, early- and mid-lactating rats and lactating rats made prolactin-deficient. Hormonal stimulation in vitro showed the maturation of response seen in vivo on transition from late pregnancy to peak lactation. Prolactin deficiency resulted in decreased release of newly synthesized lipid in response to oxytocin.
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PMID:Regulation of milk lipid secretion: effects of oxytocin, prolactin and ionomycin on triacylglycerol release from rat mammary gland slices. 894 58

The endocrine system coordinates development of the mammary gland with reproductive development and the demand of the offspring for milk. Three categories of hormones are involved. The levels of the reproductive hormones, estrogen, progesterone, placental lactogen, prolactin, and oxytocin, change during reproductive development or function and act directly on the mammary gland to bring about developmental changes or coordinate milk delivery to the offspring. Metabolic hormones, whose main role is to regulate metabolic responses to nutrient intake or stress, often have direct effects on the mammary gland as well. The important hormones in this regard are growth hormone, corticosteroids, thyroid hormone, and insulin. A third category of hormones has recently been recognized, mammary hormones. It currently includes growth hormone, prolactin, PTHrP, and leptin. Because a full-term pregnancy in early life is associated with a reduction in breast carcinogenesis, an understanding of the mechanisms by which these hormones bring about secretory differentiation may offer clues to the prevention of breast cancer.
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PMID:Hormonal regulation of mammary differentiation and milk secretion. 1216 86

Hormones have an influence on many tissues and organs, including the cardio-vascular system (CVS). Depending on their activity on CVS, they can be divided into 4 groups: having hypertensive or hypotensive influence and chronotropic positive or negative action. Endocrine regulation in CVS may occur in many ways. Apart from hormones usually connected with CVS regulation, other more recently, discovered ones can act on it. A few of these act directly through specific receptors in heart or vessel wall cells, whereas some act indirectly - stimulating other neuroendocrine factors. Additionally, novel mechanisms of signal transduction have been discovered for steroid and thyroid hormones, which are independent of gene transcription regulation and are - known as "nongenomic". Hormones which increase blood pressure include: urotensin II, endothelins, angiotensin II, catecholamines, aldosterone, antidiuretic hormone, glucocorticosteroids, thyroid hormones, growth hormone and leptin. On the other hand, blood pressure can be decreased by: natriuretic peptides, the calcitonin gene-related peptide (CGRP) family, angiotensin 1-7, substance P, neurokinin A, ghrelin, Parathyroid hormone-related protein (PTHrP), oxytocin, and, sex hormones. Hormones which when appearing in excess increase the heart rate are: catecholamines, endothelins, glucocorticosteroids, thyroid hormones, leptin and PTHrP. Those which decrease the heart rate include: natriuretic peptides, substance P, neurokinin A, oxytocin, angiotensin 1-7. This paper describes the contemporary view of the functions of hormones which act on the vessel tree and heart. The particular effect of mediator depends on many circumstances i.e.: hormone concentration, receptor type. It may also undergo contraregulation. The majority of those hormones play an important role in the pathogenesis of CVS diseases', which can result in the development of new medicines.
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PMID:[Hormones and the cardiovascular system]. 1897 53

The complex mechanisms controlling human parturition involves mother, fetus, and placenta, and stress is a key element activating a series of physiological adaptive responses. Preterm birth is a clinical syndrome that shares several characteristics with term birth. A major role for the neuroendocrine mechanisms has been proposed, and placenta/membranes are sources for neurohormones and peptides. Oxytocin (OT) is the neurohormone whose major target is uterine contractility and placenta represents a novel source that contributes to the mechanisms of parturition. The CRH/urocortin (Ucn) family is another important neuroendocrine pathway involved in term and preterm birth. The CRH/Ucn family consists of four ligands: CRH, Ucn, Ucn2, and Ucn3. These peptides have a pleyotropic function and are expressed by human placenta and fetal membranes. Uterine contractility, blood vessel tone, and immune function are influenced by CRH/Ucns during pregnancy and undergo major changes at parturition. Among the others, neurohormones, relaxin, parathyroid hormone-related protein, opioids, neurosteroids, and monoamines are expressed and secreted from placental tissues at parturition. Preterm birth is the consequence of a premature and sustained activation of endocrine and immune responses. A preterm birth evidence for a premature activation of OT secretion as well as increased maternal plasma CRH levels suggests a pathogenic role of these neurohormones. A decrease of maternal serum CRH-binding protein is a concurrent event. At midgestation, placental hypersecretion of CRH or Ucn has been proposed as a predictive marker of subsequent preterm delivery. While placenta represents the major source for CRH, fetus abundantly secretes Ucn and adrenal dehydroepiandrosterone in women with preterm birth. The relevant role of neuroendocrine mechanisms in preterm birth is sustained by basic and clinic implications.
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PMID:Neuroendocrine mechanisms in pregnancy and parturition. 2063 Oct 4