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

Oxytocin is produced in the granulosa-derived cells of the ruminant corpus luteum where its gene is dramatically up-regulated within days of ovulation. Regulation of these processes is poorly understood but oxytocin release can be increased by insulin, insulin-like growth factor I (IGF-I), and gonadotropins. Here we have assessed interactions between these regulatory systems. Follicle-stimulating hormone (FSH), luteinizing hormone (LH) and human chorionic gonadotropin (hCG) caused dose-dependent release of oxytocin from bovine granulosa cells cultured in medium containing 100 ng/ml insulin. The gonadotropins also increased oxytocin mRNA levels and their effects were mimicked by forskolin. The effects of these stimuli on oxytocin and progesterone release were synergistically increased by insulin or IGF-I. Binding studies revealed separate binding sites with characteristics of insulin and IGF-I receptors. Insulin potentiated the effects of hCG and forskolin on oxytocin mRNA levels and release of oxytocin and progesterone in cells from follicles containing greater than 50 ng/ml estradiol. In cells from follicles containing less than 5 ng/ml estradiol these stimuli had little effect on oxytocin release although progesterone release was synergistically increased by insulin and forskolin. The data suggest that gonadotropins regulate oxytocin synthesis and release and that these effects are amplified by insulin or IGF-I acting via their own receptors. Changes associated with maturation of the target cells in vitro appear prerequisite for oxytocin production in response to increased cAMP levels in the presence of insulin or IGF-I.
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PMID:Effects of gonadotropins, insulin and insulin-like growth factor I on ovarian oxytocin and progesterone production. 166 78

We have measured the effects of oxytocin and three other compounds (chlorophenyl-thio-cyclic AMP, forskolin and theophylline) that increase cytoplasmic cyclic AMP on the impedance of the toad urinary bladder. Membrane capacitance was calculated from transepithelial impedance measured by a computerized sine wave method. All four agents increased tissue capacitance. Since in these tissues this parameter is proportional to apical membrane area our results suggest that cAMP can be a second messenger involved in the action of agents that promote fusion of exocytotic vesicles with the apical membrane.
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PMID:Cyclic AMP increases electrical capacitance of apical membrane of toad urinary bladder. 172 41

This paper summarizes the recent knowledge on the factors stimulating or inhibiting the adrenocortical growth. In the part I of the present review the following stimulatory growth factors are discussed: ACTH--in vivo, N-POMC derivatives, dibutyryl cAMP--in vivo, GH, Prl, vasopressin, oxytocin, insulin, insulin-like growth factor I (somatomedin C), estradiol and vasoactive intestinal polypeptide (VIP). Among the factors, which inhibit the adrenocortical growth, the following ones are considered: ACTH--in vitro, cAMP--in vitro, adrenal steroids and testicular androgens. The remaining hormones and factors affecting the adrenocortical growth are described in the part II of the review.
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PMID:[Factors stimulating and/or inhibiting growth processes of the adrenal cortex. I. The role of the anterior pituitary and hypothalamic hormones, insulin, sex steroids and certain neuropeptides]. 194 99

Preincubation of Fura 2-loaded rat myometrial cells with H-8, an inhibitor of protein kinase A, for 1 h reversed the inhibitory effects of 8-(4-chlorophenylthio)-cAMP (CPTcAMP) on the oxytocin-stimulated increase in (Ca2+)i (intracellular free calcium), with an EC50 of 47 microM. H-8 also prevented the inhibition by relaxin and isoproterenol of the oxytocin-induced increase in (Ca2+)i. The EC50 of H-8 in reversing the relaxin effect was 42 microM. H-8 reversal of the effect of relaxin on (Ca2+)i was evident both in the absence of extracellular calcium and in cells pretreated with pertussis toxin. H-8 also reversed the inhibitory effects of relaxin and CPTcAMP on the oxytocin-induced increase in [3H]inositol phosphate formation and [3H]phosphoinositide hydrolysis. Preincubation of myometrial cells for 1 h with H-7, another protein kinase inhibitor, only partially attenuated the inhibition by relaxin and CPTcAMP of the oxytocin-induced increase in (Ca2+)i and [3H]inositol phosphate formation at concentrations 4-5 times greater than those of H-8. Acute (15-min) exposure to phorbol myristate acetate (1.0 microM) did not affect basal (Ca2+)i or the oxytocin-stimulated increases in (Ca2+)i or inositol phosphate formation. These results imply a regulatory role for protein kinase A in the inhibition of the oxytocin-induced increase in (Ca2+)i and inositol phosphate formation by relaxants.
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PMID:Involvement of protein kinase A in the regulation of intracellular free calcium and phosphoinositide turnover in rat myometrium. 196 19

Arginine (AVP) and lysine vasopressin induce a weak but statistically significant increase in the water permeability of Amoeba proteus plasmalemma. Vasotocin and deaminovasopressin, which share the hydroosmotic properties of AVP on classical vertebrate systems, are without effects on Amoeba while SKF 101926, a synthetic AVP antagonist, is even more effective than the parent compound. Theophyllin and dibutyryl-cAMP do not affect AVP action on Amoeba. Lithium, oxytocin, and carbachol are also without effect. Thus, it is unlikely that either V2 (cAMP) or V1 (phosphatidylinositol choline) receptors are involved. A clear correlation has been found between the amphiphilic character of tested peptides and their effect on Amoeba water permeability. Classical amphiphilic peptides, melittin, mastoparan, and fragment 1-8 of alpha-neoendorphin, also increased water permeability in Amoeba. It is known that vasopressin can interact with artificial lipid membranes, increasing their permeability to water. We propose that amphiphilic members of the AVP family interact directly with the lipid phase of the Amoeba membrane. Their incorporation within the lipid bilayer may cause local disruptions or may create micellar water channels as shown for other amphiphilic proteins. Our observations provide a model for the early evolution of peptide hormone systems, preceding the appearance of specific membrane receptors and associated second messenger amplifying mechanisms.
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PMID:The amphiphilic action of vasopressin and analogues on the plasma membrane of Amoeba proteus. 214 31

We examined the effects of removing extracellular Ca2+ (Ca2+e), depleting intracellular Ca2+ (Ca2+i), inhibiting cAMP-dependent calmodulin, and blocking voltage-sensitive Ca2+ channels on the secretion of ACTH by perifused dispersed rat anterior pituitary cells. The cells were stimulated with synthetic arginine vasopressin (AVP), oxytocin (OT), and angiotensin-II (AII), all of which are thought to act via the Ca2+/inositol phosphate-dependent protein kinase-C pathway, with synthetic ovine CRF, which acts via the cAMP-dependent protein kinase-A pathway, and with dioctanoylglycerol, which directly activates protein kinase-C. All three secretagogues elicited an initial spike phase ACTH secretory response that peaked within 1 or 2 min and ended within 6 min. AVP and OT also elicited a sustained plateau phase response that lasted for as long as the cells were exposed to the secretagogue, but AII did not. Removal of Ca2+e diminished the initial spike phase by 30-50%, but depletion of Ca2+i virtually abolished it. In contrast, the sustained phase of the response to AVP and OT was abolished by removal of Ca2+e. The effect of dioctanoylglycerol, which elicits a sustained progressive increase in ACTH release, but no initial spike phase, was also greatly inhibited by Ca2+e removal; no greater effect was observed when Ca2+i was depleted. Blockade of L-type voltage-sensitive Ca2+ channels with nimodipine, a dihydropyridine drug, had the same effect as Ca2+e removal on both the initial spike and sustained plateau phases of the response to AVP. Inhibiting cAMP-dependent calmodulin with penfluridol had no effect on the initial spike phase, but reduced the sustained plateau phase of the response to AVP. Removal of Ca2+e or depletion of Ca2+i did not abolish the synergistic ACTH secretory response to the combination of AVP and CRF.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Roles of intracellular and extracellular calcium in the kinetic profile of adrenocorticotropin secretion by perifused rat anterior pituitary cells. II. Arginine vasopressin, oxytocin, and angiotensin-II stimulation. 215 30

A novel relaxin sensitive cell line of apparent smooth muscle origin has been established from a newborn rhesus monkey uterus (NRMU). NRMU cells respond to relaxin, in the presence of 1 microM forskolin, by producing intracellular adenosine 3', 5'-cyclic monophosphate (cAMP). The increase in cAMP levels is dose, time and cell density dependent, reaching peak levels at 10 min when cells are seeded at 1 X 10(5) cells/well. Specificity was demonstrated by neutralization of the relaxin activity with anti-relaxin monoclonal and polyclonal antibodies, degradation of cAMP in the presence of phosphodiesterase, and confirmation of the absence of cGMP. Three synthetic analogs of human relaxin generated a dose-related cAMP response as did synthetic native human relaxin. Natural relaxin purified from human corpora lutea tissue also generated a response similar to synthetic human relaxin. Porcine and rat relaxins also increased levels of cAMP. Insulin, but not IGF I or IGF II, was capable of increasing cAMP levels in NRMU cells, however, 200 ng/mL were required to achieve cAMP levels comparable to 6.25 ng/ml relaxin. Combinations of relaxin with insulin, IGF I or IGF II did not increase cAMP levels above levels obtained with relaxin alone. The effect on NRMU cells of other hormones, growth factors and drugs potentially present in cell culture systems or serum samples was evaluated. In combination with relaxin, oxytocin significantly decreased the cAMP production below the levels induced by relaxin alone, whereas progesterone and prostaglandin E2 resulted in additive increases in cAMP. These data suggest that the NRMU cell line is an appropriate target tissue for studying relaxin-mediated biological responses in vitro as well as functioning as the primary component of a relaxin in vitro bioassay.
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PMID:Increase in cyclic AMP levels by relaxin in newborn rhesus monkey uterus cell culture. 216 18

The gene responsible for familial vasopressin-resistant nephrogenic diabetes insipidus (NDI) has been localized to a small region of the human X-chromosome (Xq28). A series of hamster lung fibroblast and mouse lymphocyte cell lines carrying fragments of the wild type human X-chromosome was analyzed for vasopressin renal-type V2 receptor expression, to test the hypothesis that the NDI locus may have identity with the V2 receptor gene. V2 receptor binding activity and induction of cAMP production in response to [Arg8] vasopressin (AVP) were exhibited by all cell lines carrying the wild type NDI locus, in contrast to control cell lines. AVP stimulation of cAMP production was concentration-dependent and could be almost completely inhibited by co-incubation with a V2-V1 receptor-specific antagonist. The V2-specific agonist [Mpa1,Val4,Sar7]AVP was as potent as AVP in inducing cAMP production by NDI-DNA-carrying cells, whereas no response was shown to other hormones such as calcitonin, oxytocin (less than 10(-8) M), isoproterenol, or an oxytocin-specific agonist. All results were consistent with the hypothesis that the V2 receptor gene co-localized with the NDI locus, supporting the view that the loci are one and the same.
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PMID:Derivatives of somatic cell hybrids which carry the human gene locus for nephrogenic diabetes insipidus (NDI) express functional vasopressin renal V2-type receptors. 216 11

The effects of morphine on arachidonic acid metabolism, on cAMP levels and on basal and induced 45Ca2(+)-uptake, in uterine strips isolated from ovariectomized rats as well as the influence of naloxone, were explored. The presence of morphine (10(-6) M) did not change significantly 14C-arachidonic acid metabolism, basal cAMP levels, or cAMP increment induced by PGE2 or by PGE1. On the other hand morphine (10(-6) M) decreased basal uterine 45Ca2(+)-uptake as much as verapamil (10(-6) M) did, and this action was not prevented by naloxone (10(-8) M). The presence of oxytocin (50 mU.ml-1) augmented 45Ca2(+)-uptake, an effect which was antagonized by morphine (10(-6) M). This inhibitory action of morphine on oxytocin-induced 45Ca2(+)-uptake was not prevented by naloxone (10(-8) M). Furthermore, PGE1 (10(-8) M and (10(-6) M) but not PGE2 (10(-8) and 10(-6) M), stimulated the incorporation of 45Ca2+ into uterine strips, and this action was not altered by morphine. The inhibitory influence of morphine on uterine spontaneous motility and on prostaglandin synthesis and release, previously described by us, is now explained in terms of an inhibition of tissue Ca2(+)-uptake.
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PMID:Effects of morphine on arachidonic acid metabolism, on Ca2(+)-uptake and on cAMP synthesis in uterine strips from spayed rats. 217 98

Current evidence suggests that oestrogens, progesterone, relaxin, the prostaglandins, and oxytocin are all hormones concerned to a major degree with the onset and maintenance of parturition. Oestrogens, relaxin, and the prostaglandins are particularly involved with cervical ripening, while prostaglandins, progesterone and oxytocin are more involved in regulating myometrial contractility. Catecholamines may also have some regulatory function in relation to uterine contractions. Progesterone dominance during pregnancy is associated with a firm closed cervix, few myometrial gap junctions, low calcium levels in the cells, and a quiescent myometrium. At term, a change in the oestrogen/progesterone balance favours cervical ripening and increased uterine activity. Of particular importance at the level of the muscle cell are changes in the number of oxytocin receptors; a complex interaction between cAMP and phosphoinositide metabolism governs the intracellular level of calcium, thus regulating contractile activity.
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PMID:The endocrinology of parturition in the human. 224 99


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