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)

The hydrosmotic response elicited by oxytocin in the frog skin epithelium (Rana esculenta) was reversibly inhibited by 70% when the medium pH was reduced to 6.2 by CO2 bubbling on the serosal side. On the contrary, the response to 8-bromo cyclic AMP (8 Br-CAMP) was not affected by medium acidification, even after corion removal. In other experiments intracellular pH was measured, employing the dimetyl-oxazolidine-dione distribution technique, in frog urinary bladder and the isolated frog skin epithelium. As previously observed in the case of oxytocin, 8 Br-CAMP increased intracellular pH in frog urinary bladder. Incubation with oxytocin also augmented the intracellular pH in the isolated frog skin epithelium but 8 Br-CAMP did not modify cell proton concentration in this tissue. From previous and present results it can be summarized that: 1) The intracellular alkalinization effect elicited by oxytocin addition and the inhibition in the hydrosmotic response induced by medium acidification were qualitatively similar in both tested target epithelia. 2) On the contrary, a post cyclic AMP step sensitive to changes in intracellular pH was not observed in frog skin, as is the case in frog urinary bladder. 3) The 8 Br-CAMP induced intracellular alkalinization effect was only observed in frog urinary bladder.
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PMID:Cellular pH and the ADH-induced hydrosmotic response in different ADH target epithelia. 644 25

In rats on day 20 of pregnancy, ONO-802 exerted a uterine contractile effect when 0.2 microgram/kg was given i.v. and also with an intrauterine administration of 0.5 ng, s.c. administration of 1 microgram/kg and vaginal administration of 10 microgram/kg. The contractile activity of ONO-802 was 100-1000 times more potent than that of PGE2 alpha and was long-acting. Intravenous PGE1 or PGE2 induced a transient contraction followed by inhibition of spontaneous uterine motility in nonpregnant rats and in those with an early pregnancy. In nonpregnant hamsters, a relaxation was seen. ONO-802, similar to PGF2 alpha, showed a contractile effect regardless of states of nonpregnancy and pregnancy, both rats and hamsters. IN rats, a contractile threshold dose of ONO-802 was similar from day 15 to day 21 of pregnancy. Oxytocin produced an acute decrease in this threshold dose on phentolamine or methysergide, but was inhibited by papaverine, dibutyryl cAMP, salbutamol and verapamil. These results suggest that uterine contraction induced by ONO-802 differs from the contractions induced by PGE1, PGE2, and oxytocin, that ONO-802 does not induce endogenous PGs, and that the effect of ONO-802 is not mediated by the autonomic nervous system.
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PMID:[Effects of 16,16-dimethyl-trans-delta 2-PGE1 methyl ester (ONO-802) on uterine motility (author's transl)]. 732 52

Myometrial tissues from pregnant rats were examined by electron microscopy for the presence of gap junctions after incubation in vitro with a variety of agents. Gap junctions were present in low frequency or absent prior to incubation in vitro. The junctions were present in control tissues in high frequency after 48 h incubation. The addition of cycloheximide or actinomycin D inhibited the incorporation of [3H]leucine into TCA-precipitable proteins and prevented gap junction formation. A prostacyclin analog (carbacyclin), a thromboxane synthesis inhibitor, and indomethacin also prevented gap junction formation. Oxytocin had no effect on gap junction formation but isoxsuprine decreased their number and increased their size. Isoxsuprine and isoproterenol also produced electron opaque crystals associated with the gap junctions. Dibutyryl cAMP treatment but not monobutyryl cGMP also increased the size of gap junctions. Based upon this and previous studies, we propose at least four sites for regulation of gap junctions and possible control of labor.
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PMID:Gap junction formation and regulation in myometrium. 743 9

The secretion of oxytocin and arginine-vasopressin was demonstrated in bovine granulosa cell culture. It was found that dbcAMP or 3-isobutyl-1-methyl-xanthine (an inhibitor of intracellular cAMP metabolization) additions increased both oxytocin and vasopressin release. The Ca2+ ionophore A23187 also stimulated, while the Ca2+ channel blocker verapamil inhibited the secretion of both nonapeptide hormones. These results suggest the involvement of cAMP- and Ca(2+)-dependent intracellular mechanisms in the stimulation of both oxytocin and vasopressin secretion by bovine granulosa cells.
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PMID:The role of cAMP- and Ca(2+)-dependent intracellular mechanisms in the control of oxytocin and vasopressin secretion by bovine ovarian granulosa cells in vitro. 753 24

Expression of the vasopressin gene appears to be a property common to all small-cell lung tumours. For some cultures of small-cell lung carcinoma (SCCL), Northern and Western Blot analyses have revealed that expression of this gene and its protein products are regulated by cAMP and glucocorticoids. In this study, these evaluations have been extended by examining the production of vasopressin-associated human neurophysin (VP-HNP) by computer-enhanced quantitative immunocytochemistry in a classical cell-line (H69) of SCCL, and defining the amount of protein in cells by area of positive staining above an arbitrarily set threshold. Intracellular cAMP was raised by incubating cells with either 8,Br-cAMP (0.5 mM) and IBMX (0.5 mM), or with forskolin (25 microM) and IBMX (0.5 mM). Both of these treatments caused a significant increase in the amount of positive VP-HNP immunoreactivity in the cells, an increase that was further enhanced by simultaneous administration of dexamethasone (0.1 microM). Addition of dexamethasone alone, however, caused a significant decrease in VP-HNP levels. Results confirm earlier findings from Western Blot analysis revealing the influence these agents have on production of vasopressin gene-related proteins by H69 cells, and indicate that computer-enhanced quantitative immunocytochemistry can be effectively used to provide a suitable index of this production.
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PMID:Factors regulating the production of vasopressin-associated human neurophysin by small-cell carcinoma of the lung: evaluation by computer-enhanced quantitative immunocytochemistry. 754 Jul 34

We investigated immunohistochemical localization of V2 vasopressin receptor along the nephron using a specific polyclonal antibody. Staining was observed in some of thick ascending limbs and all of principal and inner medullary collecting duct (IMCD) cells. Not only basolateral but also luminal membrane was stained in collecting ducts, especially in terminal IMCD (tIMCD). To learn the functional role of luminal V2 receptor in tIMCD, we studied the luminal effects of arginine vasopressin (AVP) on osmotic water permeability (Pf), urea permeability (Pu), and cAMP accumulation using isolated perfused rat tIMCD. In the absence of bath AVP, luminal AVP caused a small increase in cAMP accumulation, Pf and Pu, confirming the presence of V2 receptor in the lumen of tIMCD. In contrast, luminal AVP inhibited Pf and Pu by 30-65% in the presence of bath AVP by decreasing cAMP accumulation via V1a or oxytocin receptors and by an unknown mechanism via V2 receptors in the luminal membrane of tIMCD. These data show that V2 receptors are localized not only in the basolateral membrane but also in the luminal membrane of the distal nephron. Luminal AVP acts as a negative feedback system upon the basolateral action of AVP in tIMCD.
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PMID:Immunohistochemical localization of V2 vasopressin receptor along the nephron and functional role of luminal V2 receptor in terminal inner medullary collecting ducts. 756 68

The effect of sodium ursodeoxycholate (U) on short-circuit current (SCC), an index of basal and stimulated net ion transport across isolated skins of Bufo arenarum toads, was tested. U inhibited basal SCC when added to the epidermal side of the skins. The inhibitory effect was reversible after rinsing the preparation during 60 min. U also inhibited the natriferic response to oxytocin, db-cAMP and theophylline by 82%, 49% and 47%, respectively. Inhibition of SCC by exposure to U was reversed by the polyene antibiotic nystatin. In turn, SCC induced by nystatin in the amiloride-treated skin was insensitive to U and blocked by ouabain, a Na+, K(+)-ATPase inhibitor. These results strongly suggest that the effect of U is exerted at the apical membrane of sodium transporting cells, and rule out the existence of an additional site of inhibitory action of U.
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PMID:Inhibitory effect of sodium ursodeoxycholate on basal and stimulated short-circuit current across the isolated toad skin. 759 81

The expression of heterotrimeric (alpha beta gamma subunits) GTP-binding regulatory proteins (G proteins) and the activation of G protein-linked receptors in human granulosa cells were investigated. The cells were obtained from stimulated follicles in women undergoing in vitro fertilization and were cultured in serum-supplemented medium. Immunoblotting with specific antibodies showed that granulosa cell membranes express alpha s, alpha i3 alpha i1,2, alpha q,11 and beta subunits. Three antibodies against alpha o failed to detect this protein. The cells responded to hCG and to prostaglandin E2 with a dose-dependent increase in cAMP formation, confirming the functional activation of G alpha s. The alpha 2 adrenoceptor agonist, clonidine, inhibited hCG-stimulated cAMP formation and this effect was blocked with pertussis toxin, thus involving a Gi-type protein, most likely G alpha i2. Oxytocin provoked an increase in formation of inositol phosphates and intracellular calcium concentration, which was partly pertussis toxin resistant, providing evidence of G alpha q,11 activation. However, a significant component of the response to oxytocin could be blocked by pertussis toxin, indicating Gi-mediated phospholipase C activation (by either alpha i or beta gamma subunits). These data demonstrate the presence of G proteins in granulosa cells and suggest a complex regulation of hormonal signalling. The concentration of cAMP in these cells depended on the balance of G alpha s:G alpha i activation, whereas activation of the inositol phospholipid pathway and rises in intracellular calcium involved both Gq,11 and Gi pathways.
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PMID:G protein expression and second messenger formation in human granulosa cells. 763 9

Previous studies have demonstrated that the number of vasopressin (VP) neurons present in primary diencephalic cultures can be markedly augmented by treatment with drugs that elevate intracellular cAMP. To evaluate the effect of this drug treatment on VP secretion by hypothalamic cultures and to determine if this represents a developmental phenomenon or a mechanism involved in the continuing dynamic regulation of the VP gene, we have exposed primary dispersed hypothalamic cultures derived from 14-day-old fetal Sprague-Dawley rats to forskolin (25 microM) and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX; 500 microM), either continually or intermittently, for up to 39 days. Culture medium was collected throughout the culture period for VP RIA, and at the end of the culture period, cultures were stained immunocytochemically for neurophysin (NP). As reported by previous investigators, exposure to the drugs for 11 days resulted in an increase in the number of NP-positive neurons. The increase was sustained with longer periods of exposure up to 39 days. IBMX and forskolin treatment also resulted in detectable release of VP into the culture medium, which increased from 1.4 +/- 0.15 pg/ml at 11 days to 8.4 +/- 0.6 pg/ml after 32 days of drug treatment. The VP concentration remained undetectable (< 1.25 pg/ml) in nontreated cultures throughout this period. The effect on VP expression did not require immediate exposure to the drugs in culture, but did require the continuous presence of the drugs. Removal of the drugs from days 11-18 of culture resulted in an almost complete loss of NP-positive cells; however, reexposure to the drugs reinstated NP expression in a time-dependent fashion. The effect of IBMX/forskolin treatment on the expression of other neuronal markers was also evaluated. The treatment did not alter the total number of neurons, and there was no evidence of stimulation of oxytocin expression. There was a marked increase in the number and size of neurons stained immunocytochemically for tyrosine hydroxylase and a small increase in the number of cells staining for somatostatin. These results demonstrate that treatment with cAMP-elevating drugs markedly and selectively elevates VP secretion from dispersed hypothalamic cultures, but continuous exposure to the drugs is necessary to sustain the effect. These findings suggest that although cAMP is required in hypothalamic cultures for VP gene expression, it may also participate in the dynamic regulation of VP gene transcription in response to physiological challenges.
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PMID:The stimulation of vasopressin gene expression in cultured hypothalamic neurons by cyclic adenosine 3',5'-monophosphate is reversible. 768 52

The effects of aldosterone on sodium transport and chloride permeability were investigated by electrophysiology in two structurally distinct epithelial used as models for the distal renal tubule: the A6 cell monolayer as compared with the amphibian skin epithelium (ASE). Short-circuit current (Isc) and transepithelial conductance (Gt) were measured in A6 monolayers incubated overnight with(out) aldosterone. Cell and shunt conductances (Gcell and Gsh) were also determined, as well as the conductive nature of the chloride pathway. These parameters were correlated with sodium and chloride fluxes in A6 cells (JNa and JCl) and compared with the data recorded across ASE (Bufo marinus). The existence of a cAMP-dependent chloride secretory pathway in A6 cells was also investigated upon exposition to arginine vasopressin (AVP) or oxytocin. When A6 monolayers were incubated with aldosterone, Gt significantly increased with respect to control preparations; this increase resulted solely from an increase in Gcell, and was reflected by a 3-fold increase in Isc. There was a significant relationship between Isc and Gcell, as well as between Isc and JNa in both control and aldosterone-stimulated preparations. The A6 clone used was devoid of cAMP-dependent chloride secretory activity and was unresponsive to AVP or oxytocin. Thus, comparison between ASE and A6 preparations revealed two major differences: unlike ASE, (i) aldosterone has no effect on Gsh and (ii) no conductive reabsorptive chloride pathway is operative in A6 monolayers tested. In addition, cobalt had no effect on electrical parameters of A6 monolayers. These observations show that difference in epithelial structure is reflected in terms of electrophysiological response to aldosterone, which suggests that cell heterogeneity could be a prerequisite for observing a conductive reabsorptive chloride pathway in aldosterone-responsive, sodium-transporting epithelia.
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PMID:Aldosterone interaction on sodium transport and chloride permeability: influence of epithelial structure. 775 54


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