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)

1. The effect of (Na+ + K+)-ATPase inhibitor ouabain (10(-5)-3 x 10(-4) M), and the (Ca2+ + Mg2+)-ATPase inhibitors vanadate (6 x 10(-6)-6 x 10(-4) M), oxytocin (2 x 10(-9)-4 x 10(-8) M, and prostaglandin F2 alpha (PGF2 alpha, 10(-7)-6 x 10(-6) M) were assayed on rat uterus incubated in Ca-free medium. 2. Vanadate, oxytocin and PGF2 alpha, but not ouabain, induced contractions in a dose-dependent way (ED50: 7.5 +/- 0.03 x 10(-5) M; 6.5 +/- 0.064 x 10(-9) M and 3.8 +/- 0.085 x 10(-7) M). 3. Vanadate (3 x 10(-4) M) and oxytocin (OT, 10 mU/ml = 2 x 10(-8) M)-induced tonic contraction were not modified by nifedipine (10(-10)-10(-6) M), monensin (10(-5)-3 x 10(-4) M) or amiloride (10(-5)-10(-3) M). 4. The intracellular calcium release inhibitors TMB-8 (10(-6)-10(-4) M) and dantrolene (3 x 10(-6)-10(-4) M), and the prostaglandin release inhibitor indomethacin (3 x 10(-8)-6 x 10(-5) M) relaxed the vanadate and OT-induced tonic contractions. 5. The calmodulin inhibitors trifluoperazine (3 x 10(-5)-3 x 10(-4) M), bepridil (10(-8)-3 x 10(-4) M), calmidazolium (10(-7)-10(-4) M) and W-7 (10(-7)-10(-5) M) also relaxed the vanadate and OT-induced tonic contractions. 6. Our results suggest that oxytocin and vanadate-induced contractions on rat uterus in Ca-free medium could be produced by release of prostaglandins and intracellular calcium, and mediated by calmodulin.
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PMID:Mediators involved in the rat uterus contraction in calcium-free solution. 132 41

The characteristics of Ca(2+)-pump in smooth muscle of the rabbit small intestine were established. It was shown that Ca(2+)-pump was activated by the calmodulin and blocked by the oxytocin.
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PMID:[Ca2+-pump in myocytes of the small intestine]. 189 38

The synthesis and release of PRL are regulated by a variety of factors that originate in the hypothalamus, peripheral tissues, or posterior pituitary (PP). We recently reported that coculture of anterior pituitary (AP) and PP cells induced an increase in both PRL cell content and the responsiveness of lactotrophs to TRH. The aim of the present study was to determine whether the augmented response to TRH is due to increased lactotroph sensitivity to this particular secretagogue or to enhancement of the releasable pool of PRL. Cells obtained from anterior pituitaries of adult male rats were plated either alone or together with PP cells at the same total density. Cells cultures were maintained in serum-free medium for 4 days and then incubated for 20 min with the designated substances. Angiotensin-II and TRH evoked a significantly larger release of PRL in AP + PP cocultures than in AP cells cultured alone; the greatest difference between the culture types was observed at the highest concentrations of both secretagogues. The stimulation of PRL release by KCl, the calcium ionophore A23187, and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate was higher in the presence of PP cells than in cultures of AP cells alone, although the magnitude of this effect was lower than that seen with PRL secretagogues. The concomitant application of A23187 and 12-O-tetradecanoylphorbol-13-acetate resulted in an increased response in both types of culture and a greater relative effect of PP cells on the evoked PRL release. In contrast to other secretagogues, oxytocin (OT) elicited a smaller response in AP + PP cocultures than in AP cultures. OT was present in significant amounts in medium from cocultures, apparently after being released from the severed neuronal terminals. When AP cultures were pretreated for 4 days with comparable concentrations of OT, the acute OT-evoked PRL release was greatly diminished. These findings suggest that coculture with PP cells increases the releasable pool of PRL in lactotrophs. The stored PRL is accessible for release by secretagogues known to act via the Ca2+ second messenger system, involving both Ca2+/calmodulin and protein kinase-C pathways. The diminished response of cocultures to OT is probably due to desensitization of lactotrophs by the residual amounts of this peptide present in the disrupted nerve endings.
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PMID:Effects of coculture of anterior and posterior pituitary cells on the responsiveness of lactotrophs to different secretagogues. 193 84

The catalytic properties of myometrium sarcolemmal Ca2+, Mg2(+)-ATPase purified from plasma membrane solubilizate by affinity chromatography on calmodulin-Sepharose were investigated. The enzyme isolated in the presence of azolectin revealed a calmodulin-independent affinity for Ca2+ (Km = 0.17 microM). Purified Ca2+, Mg2(+)-ATPase displayed a strict substrate specificity, was inhibited by low concentrations of o-vanadate and was insensitive to oxytocin and prostaglandins E2 and F2 alpha. The enzyme activity was maximal at 45 degrees C, pH 7.5-8.0, and at Mg-ATP and Ca2+ concentrations of 1.5-2.5 mM and 5-20 microM, respectively.
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PMID:[Catalytic properties of purified Ca2+,Mg2+-ATPase from the myometrium sarcolemma]. 214 82

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

Ca2+/calmodulin-dependent phosphorylation of the 20-kDa regulatory light chain of myosin is of signal importance in the initiation of contraction in a number of smooth muscle tissues. In this investigation, we evaluated the relationship between intracellular free Ca2+/concentration [( Ca2+]i) and the extent of myosin light chain phosphorylation in cultured human myometrial smooth muscle cells. Treatment of myometrial cells with ionomycin caused a concentration- and time-dependent increase in [Ca2+]i and phosphorylation of myosin light chain. Temporally, the increases in light chain phosphorylation and [Ca2+]i in response to ionomycin were similar. In myometrial cells treated with ionomycin (10(-5) M) for 10 s, [Ca2+]i increased from 138 to 800 nM; in these same cells, myosin light chain phosphorylation increased from 5% to a maximum value of 54%. Half-maximal phosphorylation of myosin light chain was attained at 300 nM [Ca2+]i. Treatment of myometrial smooth muscle cells with prostaglandin (PG) F2 alpha (10(-8) M) and PGE2 (10(-8) M) caused a proportionate increase in [Ca2+]i and myosin light chain phosphorylation. In addition, [Ca2+]i and myosin light chain phosphorylation increased in response to oxytocin and angiotensin II. These findings indicate that a number of uterotonic agents effect an increase in [Ca2+]i, which in turn causes phosphorylation of myosin light chain. Furthermore, the concentration of Ca2+ in the cytoplasm is a primary determinant for myosin light chain phosphorylation in human myometrial smooth muscle cells.
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PMID:Myosin light chain phosphorylation in human myometrial smooth muscle cells. 230 67

1. Isolated nerve endings from rat neurohypophyses were permeabilized with digitonin in order to gain access to the cytoplasm. Release of vasopressin (AVP), oxytocin and the neurophysins was studied under different experimental conditions. 2. Hormone release, which occurred by exocytosis, was Ca2+ dependent. Half-maximal release was observed at ca. 1.7 microM-Ca2+ in contrast to ca. 300 microM for K+-induced hormone secretion from non-permeabilized neurosecretosomes. 3. Release also occurred when the neurosecretosomes were challenged with Ca2+ 20 min after digitonin treatment. This suggests that the isolated nerve endings remain permeable after treatment with digitonin. 4. Although hormone release was potentiated in the presence of ATP, and to a lesser extent with guanosine triphosphate (GTP), secretion occurred in the absence of nucleotides. 5. Replacement of K+ as the major cation by Na+ did not modify the secretory response to a Ca2+ challenge. Release, although reduced, still occurred when KCl was replaced by sucrose. 6. Compared to glutamate, Cl-, Br- and I- did not modify the Ca2+-independent release. This release was increased in the presence of SCN-. The order of effectiveness of the anions studied in inhibiting the Ca2+-dependent release was glutamate less than Br- = Cl- = I- less than SCN-. 7. Increasing the osmolarity of the perfusate inhibited the Ca2+-dependent release of AVP and oxytocin. 8. Vincristine, which binds to microtubules, had no effect on the secretory process. 9. Ca2+ dependent AVP release was partially inhibited by the calmodulin antagonist trifluoroperazine. 10. Hormone release was potentiated by the protein kinase C activator, 4-beta-phorbol 12-myristate acetate (TPA). 11. Whereas 0.2 microM-Ca2+ induced a barely significant increase in AVP release, inositol 1,4,5-triphosphate, in the continued presence of 0.2 microM-Ca2+, produced a large secretory response. 12. 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS), an inhibitor of Cl- permeability, reduced the Ca2+-dependent AVP release. 13. Carbonyl cyanide m-chlorophenylhydrazone (CCCP), which reduces the transmembrane potential of isolated neurohypophysial granules, inhibited the Ca2+-dependent hormone secretion. 14. Maximal hormone release occurred at pH 6.6. 15. It is concluded that the permeabilized neurosecretosomes represent an excellent model for studying the minimal requirements for neurosecretion.
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PMID:Requirements for hormone release from permeabilized nerve endings isolated from the rat neurohypophysis. 245 Oct

The effect of oxytocin on phosphoinositide metabolism as well as on membrane protein phosphorylation in myometrial tissue was studied. Oxytocin enhanced the 32P incorporation into phospholipids in myometrial tissue. The effect of oxytocin on phosphoinositide metabolism was also detected in plasma membrane of 20 days pregnant rats. Phosphorylated membrane lipids have been analysed and phosphatidylinositol 4, 5-bisphosphate proved to be the main reaction product. Oxytocin enhanced the 32P incorporation into phospholipids measured in the first 30 sec then the labeling decreased more rapidly then in case of the control. The effect of oxytocin proved to be concentration dependent. The protein phosphorylation was also influenced by oxytocin. However the amount of alkylphosphate formed depended on the presence or absence of Ca2+, Ca2+-calmodulin and cyclic AMP, oxytocin influenced the protein phosphorylation in the presence of Ca2+-calmodulin only.
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PMID:Oxytocin regulates Ca2+ level in myometrium by influencing phosphoinositide metabolism. 255 23

Nafazatrom inhibits, in a dose-dependent way, the amplitude and frequency of the rhythmic contractions induced by oxytocin (4 mU/ml), as well as the methacholine (10(-5) M)- and CaCl2 (10 mM)-induced contractions, and the phasic response to KCl (60 mM); similarly, it inhibits the tonic contraction induced by KCl (60 mM) and oxytocin (10 mU/ml). A single concentration of nafazatrom (10(-4) M) also inhibits the uterine contractions caused by carbachol (10(-4) M) and prostaglandin F2 alpha (10(-6) M). CaCl2 (0.1-10 mM) only partially reverses the inhibition produced by nafazatrom on the KCl-induced tonic contractions. Bay K 8644 (3 x 10(-10)-3 x 10(-7) M) reverses the inhibition by 10(-4) M but not by 3 x 10(-4) M of nafazatrom on the CaCl2-induced contractions. Nafazatrom also inhibits, in a dose-dependent way, the calmodulin-dependent phosphodiesterase activity. Our results would suggest that, independently of its 5-lipoxygenase blocking activity, nafazatrom inhibits the contractions of the rat uterus by inhibiting the calmodulin activity and, presumably, by reducing the influx of extracellular calcium and/or the mobilization of intracellular calcium.
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PMID:Mechanism of nafazatrom-induced inhibition of rat uterus contractions in vitro. 256 Mar 65

This study explored an effector mechanism associated with the arginine vasopressin (AVP) recognition site in the hippocampus, namely, potentiation of norepinephrine (NE)-induced cAMP accumulation in the surviving hippocampal slice. The biochemical mechanisms that underlie the AVP potentiation were investigated as follows: First, the actions of AVP upon NE-induced accumulation of cAMP in hippocampal slices from rat brain were specific to AVP and not shared by other closely related peptides, namely, oxytocin and AVP4-9. Second, the AVP-induced neuromodulation involved beta-adrenergic receptors, with AVP having no effect on cAMP levels in the absence of NE. Third, the potentiation by AVP was biphasic, with lower AVP concentrations potentiating NE-induced cAMP accumulation, while higher concentrations did not potentiate. Fourth, an antagonist of V1-type AVP receptors blocked AVP potentiation. Fifth, AVP potentiation was dependent upon extracellular calcium concentrations. Sixth, AVP potentiation was blocked by 50 microM trifluoperazine, which is consistent with a calcium-calmodulin involvement but which might also implicate protein kinase C. These alternatives and the nature of the calcium involvement are discussed. AVP actions thus appear to involve interactions between several second-messenger systems and suggest a biochemical mechanism by which AVP exerts its centrally mediated behavioral effects.
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PMID:Vasopressin neuromodulation in the hippocampus. 256 30


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