UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumors of the female genital tract may be associated with a variety of unusual clinical manifestations. Uncommon endocrine and paraendocrine syndromes include production of human chorionic gonadotropin by tumors other than those of germ cell origin, hyperthyroidism associated with struma ovarii and gestational trophoblastic disease, the carcinoid syndrome, the Zollinger-Ellison syndrome, hypercalcemia, Cushing's syndrome, hypoglycemia, hypertension related to renin or aldosterone production, hyperprolactinemia, inappropriate secretion of antidiuretic hormone, and virilization associated with Nelson's syndrome and placental site trophoblastic tumor. Paraneoplastic syndromes associated with gynecological tumors include disorders of the nervous system, connective tissue, and skin, as well as hematologic abnormalities and the nephrotic syndrome. Heritable and other congenital syndromes associated with these tumors are the Peutz-Jeghers syndrome, the nevoid basal-cell carcinoma syndrome, Ollier's disease and Maffucci's syndrome, hereditary leiomyomatosis, ataxia-telangiectasia, von Hippel-Lindau's disease, thyroid abnormalities associated with Sertoli-Leydig cell tumors, and Carney's complex. Other syndromes associated with tumors of the female genital tract include Meigs' syndrome, hyperamylasemia, uveal melanocytic lesions, and pyrexia.
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PMID:Clinical syndromes associated with tumors of the female genital tract. 175 57

Immunochemical studies associated with physicochemical procedures led to demonstrate the presence of neurohypophysial-like peptides in the testis of numerous species including human. Characterization of arginine-vasopressin-neurophysin II mRNA and oxytocin-neurophysin I mRNA in rat testicular extracts is in favour of a local production for these peptides. The in vitro and in vivo evidences of a direct regulation of testicular steroidogenesis bg AVP and related peptides--the identification of specific AVP receptors on purified Leydig cells and their alteration in some physiological or pathological situations argue for a paracrine/autocrine role of these neurohypophysial-like-peptides in modulating Leydig cell androgen biosynthesis.
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PMID:[Intragonadal control of testicular function by neurohypophyseal-like peptides]. 213 Jul 61

Luteinizing hormone is the major regulator of Leydig cell differentiation and steroidogenic function. A number of hormones produced by the Leydig cell (e.g. estrogen, angiotensin, CRF, vasopressin) and the tubular compartment (inhibin, TGF beta), can influence both acute and long-term actions of LH. Conversely, hormones produced in the Leydig cells modulate tubular function (e.g. androgen, beta-endorphin, oxytocin). The LH stimulatory event can be negatively influenced by the action of angiotensin II through the guanyl nucleotide inhibitory unit of adenylate cyclase. We have recently discovered an action of corticotrophin releasing hormone through specific high-affinity low-capacity receptors in the Leydig cells which involves a pertussis toxin insensitive guanyl nucleotide regulatory unit with interaction between signalling pathways and resulting inhibition of LH induced cAMP generation and consequently of steroidogenesis. In contrast to other tissues the CRF receptor in the Leydig cells did not couple to Gs. CRF action is exerted through direct or indirect action of protein kinase C, at the level of the catalytic subunit of adenylate cyclase. Physiological increases in endogenous LH cause positive regulation of membrane receptors and steroidogenesis, while major elevations in circulating gonadotropin can induce down-regulation of LH receptors and desensitization of steroid responses in the adult cell. Gonadotropin-induced desensitization in adult rat tests include an estrogen mediated steroidogenic lesion of the microsomal enzymes 17 alpha-hydroxylase/17,20-desmolase. For further understanding of the regulation of this key enzyme of the androgen pathway the rat P450(17) alpha cDNA was cloned and sequenced. This cDNA expressed in COS-1 cells 17 alpha-hydroxylase/17,20-desmolase activities. From the deduced amino acid sequence, two transmembrane regions were identified, a signal peptide for insertion in the ER, and a 2nd transmembrane region separated from the first by 122 amino acids. The carboxy terminal non-transmembrane region possesses 4 hydrophobic clefts, of which cleft II would contain the putative steroid binding site for both hydroxylase and lyase activities. The rat cDNA was employed to evaluate the hormonal regulation of mRNA levels in adult and fetal Leydig cells. Low dose hCG treatment caused an early increase in mRNA levels followed by a return to control values at later times, while with higher desensitizing doses the initial increase in mRNA was followed by a marked reduction in mRNA at 24 h and a small recovery at 48 h. Fetal rat Leydig cells treated with E2 showed a 70% decrease in P450 mRNA levels, and testosterone production closely followed the changes in mRNA.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:LH action in the Leydig cell: modulation by angiotensin II and corticotropin releasing hormone, and regulation of P450(17) alpha mRNA. 269 45

We have previously shown that testicular fluid contains factors that can inhibit luteinizing hormone (LH)-stimulated androgen production by Leydig cells, and others have reported the presence of immunoreactive vasopressin (iAVP) in the testes as well as in vitro inhibition by vasopressin of Leydig cell-androgen production. In the current report, we have used an established radioimmunoassay (RIA) to measure the concentration of iAVP in testicular fluid and have related changes in iAVP concentration to disruption of the seminiferous tubules. Spermatogenesis was disrupted in adult rats by surgically establishing bilateral cryptorchidism. The concentration of iAVP decreased progressively from 349 +/- 52 to 61 +/- 5 pg/ml during 4 wk. When cryptorchidism was unilaterally established, the concentration of iAVP in fluid from that testis decreased to 116 +/- 19 pg/ml while the concentration of iAVP in the contralateral scrotal testis remained unaffected. Unilateral ligation of the ductuli efferentes also caused an equivalent unilateral decrease in iAVP to 110 +/- 15 pg/ml. The osmotic pressure of the testicular fluid was not altered by disruption of gametogenesis, and the extracellular "albumin space" was not increased. Therefore, the decrease in concentration of iAVP was probably not due to dilution with increased amounts of interstitial fluid. We conclude that the disruption of spermatogenesis is associated with a decrease in the concentration of iAVP in testicular fluid and suggest that AVP or a similar peptide may be involved in the intratesticular mechanisms associated with increased production of androgen by Leydig cells after disruption of spermatogenesis.
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PMID:Disruption of spermatogenesis is associated with decreased concentration of immunoreactive arginine vasopressin in testicular fluid. 290 83

We have previously shown that arginine vasopressin (AVP) directly inhibits testicular steroidogenesis in vitro. In the present study, binding of neurohypophysial peptides to interstitial cells of the rat testis was studied using [3H]AVP as the ligand. Interstitial cells were obtained from adult rat testis after collagenase dispersion and were incubated with [3H]AVP in the presence or absence of unlabeled AVP. Binding equilibrium was reached by 60 min at 4 C, while incubation at higher temperatures (23 and 37 C) resulted in an apparent decrease in binding. Scatchard plot analysis of equilibrium binding data revealed the existence of one class of high affinity, low capacity binding sites (Kd = 1.0 +/- 0.3 nM; maximal binding = 8.5 fmol/10(6) cells). In addition, the rate constants of association and dissociation were calculated to be 0.024 nM-1 min-1 and 0.009 min-1, respectively. Addition of naturally occurring neurohypophysial hormones as well as their synthetic analogs inhibited [3H]AVP binding to testis cells, resulting in parallel displacement curves. The order of potencies for the native peptides was: AVP = lysine vasopressin = arginine vasotocin (IC50, 5 X 10(-10) M) greater than oxytocin = mesotocin (IC50, 4 X 10(-7) M) greater than isotocin = glumitocin (IC50 greater than 10(-6) M). Furthermore, two potent vasopressor antagonists, d(CH2)5Tyr(Me)AVP ([1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]AVP) and dPTyr(Me)AVP ([1-deaminopenicillamine-2-(O-methyl)tyrosine]AVP) competed for [3H]AVP binding with a higher affinity (IC50, approximately 10(-11) M) than native AVP. In contrast, a selective antidiuretic agonist, dDAVP (1-deamino-8-D-AVP), only competed weakly for receptor binding, while a specific oxytocic agonist, (Thr4,Gly7)oxytocin, did not affect AVP binding. These results suggested that the testis may contain the V1 receptor subtype. Studies on the intratesticular distribution of AVP receptors indicated minimal binding to cells derived from the seminiferous tubule, while most of the AVP-binding sites sediment with enriched fractions of Leydig cells after Metrizamide density gradient centrifugation. AVP-binding sites were also found in rat liver, kidney, and anterior pituitary (10.7, 2.6, and 1.7 fmol/mg protein), whereas adrenal, cerebellum, prostate, and hypothalamus were devoid of AVP-binding sites. Thus, we have demonstrated the presence of high affinity, stereospecific receptors for AVP in the interstitial cell compartment of the rat testis. These V1 receptors may mediate the direct inhibitory action of neurohypophysial hormones on testicular Leydig cell steroidogenesis.
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PMID:Identification and characterization of arginine vasopressin receptors in the rat testis. 298 Oct 73

The effect of human chorionic gonadotropin (hCG) on intact Leydig cell phospholipid methylation was studied. Hormonal stimulation of rat Leydig cells increased the incorporation of [methyl-3H]methionine into phospholipids threefold. This effect was observed after 10 minutes of incubation time and was time and dose dependent with a maximal stimulation at 67 ng/ml of hCG. In the presence of hCG, 3H-labeled methyl groups were preferentially incorporated into phosphatidyl-N-monomethylethanolamine. This effect of hCG was not reproduced by dibutyryl cyclic adenosine monophosphate (cAMP), cholera toxin, or forskolin. Purified hCG beta subunit but not hCG alpha subunit had stimulatory activity on Leydig cell phospholipid methylation. We conclude that luteinizing hormone (LH)/hCG stimulates specifically Leydig cell phospholipid methylation, because LH-releasing hormone or [Arg8]-vasopressin did not modify these reactions. We postulate that these reactions are occurring at a cellular level that involves hormone-receptor interaction. It is also suggested that this biological response involves hCG beta subunit receptor interaction and does not require cAMP synthesis.
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PMID:Human chorionic gonadotropin and free beta subunits stimulate phospholipid methylation in intact rat Leydig cells. 769 25

The influence of spent medium from immature mouse Sertoli cells (SCM) on testosterone production by purified Leydig cells was investigated and compared to that of AVP, a potent local modulator of Leydig cell steroidogenesis. SCM inhibited in a dose-dependent manner the hCG-stimulated testosterone production, but was ineffective in basal conditions. As is known for AVP, (i) a lag period of 72 h was prerequisite for SCM to inhibit Leydig cell function; (ii) the main effect of SCM was located at a step beyond the receptor-adenylate cyclase system, since the hCG- and 8-bromo-cAMP-stimulated testosterone productions were similarly affected. The possibility that the effect of SCM may be related to AVP-like molecule(s) is also supported by the observations that at maximal concentrations the inhibitory effects of AVP and SCM were not additive and that the inhibition of testosterone production was largely (65%) reversed by the presence of [(beta-mercapto-beta, beta-cyclopentamethylenepropionyl, O-Me-Tyr2,Arg8)-vasopressin], a selective vasopressor antagonist. These data indicate that Sertoli cells produce in vitro potent inhibitory factors of Leydig cell steroidogenesis. They provide additional evidence that one of these bioactive factors has an effect on Leydig cell function similar to that of AVP.
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PMID:Presence in mouse Sertoli cell-conditioned medium of a factor that expresses AVP-like inhibition of steroidogenesis by mouse Leydig cells in long-term culture. 818 58

Relaxin is a 6-kDa peptide of the insulin family that is present at increased levels in the circulation during pregnancy. Its functions at that time are thought to include maintenance of myometrial quiescence, regulation of plasma volume, and release of neuropeptides, such as oxytocin and vasopressin. The protein also promotes connective tissue remodeling, which allows cervical ripening and separation of the pelvic symphysis in various mammalian species. In this report, we provide evidence for a novel target of relaxin, the human monocytic cell line, THP-1. Relaxin bound with high affinity (Kd = 102 pM) to a specific receptor on THP-1 cells. Receptor density was low ( approximately 275 receptors/cell), but binding of relaxin triggered intracellular signaling events. Receptor density was not modulated by pretreatment with estrogen, progesterone, or a number of other agents known to induce differentiation of THP-1 cells. Cross-linking studies showed radiolabeled relaxin bound primarily to cell surface proteins with an apparent molecular mass of >200 kDa. Other members of the insulin-like family of proteins (insulin, insulin-like growth factors I and II, and relaxin-like factor) were unable to displace the binding of relaxin to THP-1 cells, suggesting that a distinct receptor for relaxin exists on this monocyte/macrophage cell line.
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PMID:Relaxin binds to and elicits a response from cells of the human monocytic cell line, THP-1. 891 Mar 95

The mechanism of arginine vasopressin (AVP) action in Leydig cells was investigated, and compared to the effects of phorbol-13-myristate-12-acetate (PMA) and interleukin-1 beta (IL-1 beta). Previous reports suggested that AVP inhibits Leydig cell testosterone production at the level of 17 alpha-hydroxylase/C17-lyase activity. The present study confirms and extends these observations, and contrasts the effects of AVP to IL-1. In all experiments, macrophage-depleted Leydig cells were isolated from mice and maintained in primary culture for 5 d prior to initiation of treatments. Leydig cells were treated with 8-Br-cAMP plus increasing concentrations of AVP or IL-1 beta. AVP caused a significant and dose-dependent inhibition of cAMP-stimulated testosterone production and P450c17 mRNA expression. IL-1 beta completely inhibited cAMP-stimulated testosterone production and P450c17 mRNA expression. PMA is a known activator of protein kinase C (PKC) and has been reported to inhibit Leydig cell steroidogenesis. Leydig cells express type V1 vasopressin receptors, which are coupled to PKC activation. The mechanism of IL-1 action in Leydig cells is not understood, but activation of the PKC pathway has been suggested for IL-1 action in other systems. Therefore, the effects of PMA on cAMP-stimulated steroidogenesis were compared to AVP and IL-1. Similar to the effects of AVP, PMA inhibited cAMP-stimulated testosterone production and P450c17 mRNA expression. To assess the possible involvement of PKC in AVP and IL-1 action in Leydig cells, the PKC inhibitor Calphostin C was tested. cAMP-stimulated testosterone production and P450c17 mRNA expression were significantly inhibited by 10 nM AVP (p < 0.05), and this inhibition was reversed by treatment with Calphostin C. Analogous experiments were performed to assess the role of PKC in IL-1 action. In contrast to the results for AVP, Calphostin C did not reverse the inhibitory effects of IL-1 on cAMP-stimulated P450c17 mRNA expression. To assess further PKC activation, myristoylated alanine-rich C kinase substrate (MARCKS) phosphorylation was analyzed. Only AVP and PMA, but not IL-1 beta, caused an increase in MARCKS phosphorylation. These results confirm that AVP and PMA activate PKC and indicate that IL-1 likely does not activate PKC in Leydig cells. The implications of AVP-mediated inhibition of steroidogenesis and potential role of MARCKS phosphorylation are discussed.
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PMID:Arginine vasopressin inhibition of cytochrome P450c17 and testosterone production in mouse Leydig cells. 966 41

Rat Leydig cells contain a phospholipase D (PLD), which can be activated by vasopressin and phorbol ester. In order to clarify which Leydig cell organelles that express PLD activity, the subcellular localization of two differently regulated PLD activities was investigated by subcellular fractionation on a 40% (v/v) self-generating Percoll gradient. PLD activities in broken cells were estimated using radiolabeled didecanoylphosphatidylcholine as a substrate. Initial experiments revealed the presence of an oleate Mg2+ -activated PLD and a phosphatidylinositol 4,5-bisphosphate-activated PLD (PIP2-PLD) in the microsomal fraction of Leydig cells. The latter activity could be further stimulated by recombinant nonmyristoylated ADP ribosylating factor 1 (ARF1) plus GTPgammaS. The peak of oleate Mg2+ -PLD activity colocalized with the plasma membrane marker, whereas the highest specific activity of the PIP2-PLD activity was found in fractions with a slightly lower density than those containing the plasma membrane and trans-Golgi marker enzymes. In order to localize phorbol ester-stimulated PLD activity in intact Leydig cells, the cells were prelabeled with [14C]-palmitate and then stimulated for 15 min with 100 nM 4-beta-phorbol-12-myristate-13-acetate (PMA) in the presence of ethanol or butanol. The PLD product [14C]-phosphatidylethanol, expressed as the percentage of total labeled phospholipids in the fraction, was slightly increased in all Percoll fractions and showed a prominent peak in the fractions containing plasma membrane, trans-Golgi, and fractions of slightly lower density. The PMA-induced formation of [14C]-phosphatidylbutanol could be inhibited dose-dependently with brefeldin A suggesting that the activation of PLD by the phorbol ester was mediated by ARF.
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PMID:The subcellular localization of phospholipase D activities in rat Leydig cells. 1043 28

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