Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study tested for the presence of androgen receptor-immunoreactivity in somatostatin, galanin, vasopressin, corticotropin-releasing hormone, and oxytocin neurons in the rat forebrain. The brains of adult male Sprague-Dawley rats were fixed with 4% paraformaldehyde. Androgen receptor was visualized in coronal sections using nickel intensification of diaminobenzidine, and the neuropeptides were identified using a brown diaminobenzidine reaction product. Androgen receptor was localized to the nuclei of neurons in the septum, amygdala, cortex, hippocampus, and hypothalamus. The majority of somatostatin-containing neurons in the periventricular hypothalamic nucleus also contained androgen receptor. Androgen receptor was also found within galanin-expressing cells in the bed nucleus of the stria terminalis and in the amygdala. Androgen receptor was not observed in corticotropin-releasing hormone, vasopressin, or oxytocin neurons in all areas examined. The data suggest that androgens may be capable of directly regulating somatostatin-expressing neurons of the periventricular nucleus of the hypothalamus and galanin-containing neurons of the bed nucleus of the stria terminalis and amygdala.
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PMID:Localization of androgen receptor within peptidergic neurons of the rat forebrain. 785 Apr 90

Most cases of congenital nephrogenic diabetes insipidus (NDI) are inherited in an X-linked manner, which is due to the mutations of the vasopressin type 2 receptor (V2R) gene. However, recent reports have presented female NDI patients with heterozygote V2R gene mutations. The mechanism of inheritance was thought to be skewed X-inactivation. We present a family with congenital NDI. Three male members were diagnosed with NDI, and examination of their V2R gene revealed a G inserted at nucleotide 804 of the open reading frame. Three female individuals display different degrees of symptoms of NDI, and all of them possess both the normal and abnormal genes. The X-inactivation patterns of the female members were investigated via the detection of methylated trinucleotide repeat in the human androgen receptor gene. The grandmother showed extremely skewed methylation of one X chromosome, and the mother revealed moderately skewed methylation. The daughter of the grandmother's sister, who has no symptoms of NDI, showed random methylation. The highly skewed X-inactivation pattern of the grandmother suggests that her NDI phenotype is caused by dominant methylation of the normal allele of V2R gene.
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PMID:Detection of skewed X-inactivation in two female carriers of vasopressin type 2 receptor gene mutation. 932 82

Contractions of rat thoracic aorta to vasopressin (VP) are threefold higher in females (F) than in males (M), primarily because nitric oxide (NO) attenuation of contraction is greater in M. To determine the role of the androgen receptor (AR) in this mechanism, vascular reactivity to VP was examined in thoracic aorta of the testicular-feminized male (Tfm) rat, which has an X-linked, recessive defect in AR function in affected M. Maximal contraction of normal aortas to VP was fourfold higher in F (4,128 +/- 291 mg/mg ring wt) than in M (971 +/- 133 mg); maximal response of Tfm (3,967 +/- 253 mg) was similar to that of normal F. N(G)-nitro-L-arginine methyl ester increased maximal response to VP threefold in M but had no effect in F or Tfm. In contrast, maximal contraction of normal aortas to phenylephrine was 43% higher in M (4,011 +/- 179 mg) than in F (2,809 +/- 78 mg); maximal response of Tfm (2,716 +/- 126 mg) was similar to that of normal F. N(G)-nitro-L-arginine methyl ester increased maximal response to phenylephrine by >50% in F and Tfm but had no effect in M. Maximal contractile response to 80 mM KCl did not differ among M, F, or Tfm. Thus androgens and normal vascular AR function are important in the greater NO-mediated attenuation of reactivity to VP in M than in F rat aorta, which may involve specific modulation of endothelial VP signal transduction pathways and NO release by androgens. These data also establish the importance of the Tfm rat as a model to study the effects of androgens on cardiovascular function.
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PMID:Androgen-receptor defect abolishes sex differences in nitric oxide and reactivity to vasopressin in rat aorta. 1171 25

X-linked nephrogenic diabetes insipidus (NDI) is a rare inherited disorder caused by mutations in the arginine vasopressin receptor 2 (V2R) gene. The clinical phenotype is fully expressed in hemizygous male patients and is usually asymptomatic in heterozygous females. In the present study, a 51-yr-old Japanese female with congenital NDI and her family members were examined. The patient developed severe hypernatremia accompanied by hypoosmotic polyuria after gynecological surgery, and was unable to concentrate urinary osmolality in response to exogenous vasopressin. Direct sequencing analysis of the propositus and her two affected sons revealed a two-nucleotide deletion change at codon 30 (g.452-453delAC) in the V2R gene, resulting in a frameshift and premature termination in translation at codon 190. The X chromosome inactivation pattern was investigated in the propositus using methylation analysis of the polymorphic CAG repeat in the androgen receptor gene, and the value for relative X chromosome inactivation of one allele was 70.2%. In conclusion, we identified a novel V2R gene mutation in a female patient and her sons with congenital NDI, and her phenotype may be caused by skewed X chromosome inactivation.
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PMID:A novel deletion mutation in the arginine vasopressin receptor 2 gene and skewed X chromosome inactivation in a female patient with congenital nephrogenic diabetes insipidus. 1512 13

The steroid sensitive vasopressin cells of the bed nucleus of the stria terminalis (BST) and centromedial amygdala (CMA) are involved in numerous behavioural and physiological functions. These cells are known to be greatly influenced by gonadal steroids. Castration reduces and testosterone replacement restores arginine vasopressin (AVP)-immunoreactive (-ir) labelling and AVP mRNA expression in the BST and CMA. Gonadal steroids appear to act directly in AVP-expressing cells within the BST and CMA, because the majority of AVP-ir cells in these areas contain oestrogen and androgen receptor immunoreactivity. Recently, we have localised progestin receptor immunoreactivity in virtually all of the AVP-ir cells in the BST and CMA. To understand the role played by progestin receptors in AVP cells within the BST and CMA, we treated male rats with 1 mg of progesterone or oil for 5 days, and then examined AVP immunoreactivity within the brain. We found that progesterone decreased AVP-ir labelling within the BST and CMA, as well as in two of the projection sites of these cells, the lateral septum and lateral habenula. Progesterone treatment did not alter testosterone secretion from the testes, nor did it alter adult male sexual behaviour. These data illustrate an additional mechanism by which the AVP cells in the BST and CMA can be regulated. These data also suggest that progesterone may act in the male brain to influence behaviours that are AVP-dependent.
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PMID:Progesterone treatment of adult male rats suppresses arginine vasopressin expression in the bed nucleus of the stria terminalis and the centromedial amygdala. 1645 2

Androgens and the androgen receptor (AR) play important roles in the testes. Previously we have shown that male total AR knockout (T-AR-/y) mice revealed incomplete germ cell development and lowered serum testosterone levels, which resulted in azoospermia and infertility. However, the consequences of AR loss in particular types of testicular cells remain unclear. Using a Cre-loxP conditional knockout strategy, we generated a tissue-selective knockout mouse with the AR gene deleted in testis peritubular myoid cells (PM-AR-/y). Phenotype analyses showed that PM-AR-/y mice were indistinguishable from WT AR (AR+/y) mice with the exception of smaller testes size. PM-AR-/y mice have serum testosterone concentrations comparable with AR+/y mice. PM-AR-/y mice have oligozoospermia in the epididymis; however, fertility was normal. Although normal germ cell distribution ratio was found, total germ cell number decreased in PM-AR-/y mice. Further mechanistic studies demonstrated that PM-AR-/y mice have defects in the expression of Sertoli cells' functional marker genes such as tranferrin, epidermal fatty acid-binding protein, androgen-binding protein, and other junction genes including occludin, testin, nectin, zyxin, vinculin, laminingamma3, gelsolin, connection43, and N-cadherin. Furthermore, there were defects in peritubular myoid cell contractility-related genes such as endothelin-1, endothelin receptor A and B, adrenomedullin, adrenomedullin receptor, and vasopressin receptor 1a. Together, our PM-AR-/y mice provide in vivo evidence for the requirement of functional AR in peritubular myoid cells to maintain normal Sertoli cells function and peritubular myoid cell contractility, thus ensuring normal spermatogenesis and sperm output.
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PMID:Oligozoospermia with normal fertility in male mice lacking the androgen receptor in testis peritubular myoid cells. 1709

About 90% of patients with congenital nephrogenic diabetes insipidus (NDI) have vasopressin type 2 receptor (V2R) gene mutations that are inherited in an X-linked recessive manner. Although most female carriers are asymptomatic, some female carriers show polydipsia and polyuria. The reason why female carriers show NDI symptoms is explained by skewed X-inactivation. We studied X-inactivation patterns of six female carriers with heterozygote V2R gene mutations. The X-inactivation pattern in peripheral blood leukocytes was examined using methylation analysis of the polymorphic CAG repeat in the androgen receptor gene. Two asymptomatic female carriers showed random X-inactivation (61.9% and 60.7%). Skewed X-inactivation patterns (71.6%, 79.4%, and 91.2%) occurring preferentially to normal X alleles were recognized in three female carriers who showed clinical NDI symptoms. However, in one female carrier who showed clinical NDI symptoms, random X-inactivation (55.4%) was recognized. In conclusion, the clinical NDI phenotypes may correlate with the X-inactivation patterns in female carriers with heterozygote V2R gene mutations. However, in some female carriers, we cannot predict the clinical phenotypes by the evaluation of the X-inactivation patterns in peripheral blood leukocytes, because X-inactivation ratios within an individual are sometimes different between tissues.
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PMID:Correlation between clinical phenotypes and X-inactivation patterns in six female carriers with heterozygote vasopressin type 2 receptor gene mutations. 1832 75

Hyperactivity of corticotropin-releasing factor (CRF) neurons in the paraventricular nucleus (PVN) of the hypothalamus is a prominent feature in depression and may be important in the etiology of this disease. The activity of the CRF neurons in the stress response is modulated by a number of factors that stimulate or inhibit CRF expression, including (1) corticosteroid receptors and their chaperones, heat shock proteins 70 and 90, (2) sex hormone receptors, (3) CRF receptors 1 (CRFR1) and 2, (4) cytokines interleukin 1-beta and tumor necrosis factor-alpha, (5) neuropeptides and receptors, vasopressin (AVP), AVP receptor 1a (AVPR1A) and oxytocin and (6) transcription factor cAMP-response element-binding protein. We hypothesized that, in depression, the transcript levels of those genes that are involved in the activation of the hypothalamo-pituitary-adrenal (HPA) axis are upregulated, whereas the transcript levels of the genes involved in the inhibition of the HPA axis are downregulated. We performed laser microdissection and real-time PCR in the PVN and as a control in the supraoptic nucleus. Snap-frozen post-mortem hypothalami of seven depressed and seven matched controls were used. We found significantly increased CRF mRNA levels in the PVN of the depressed patients. This was accompanied by a significantly increased expression of four genes that are involved in the activation of CRF neurons, that is, CRFR1, estrogen receptor-alpha, AVPR1A and mineralocorticoid receptor, while the expression of the androgen receptor mRNA involved in the inhibition of CRF neurons was decreased significantly. These findings raise the possibility that a disturbed balance in the production of receptors may contribute to the activation of the HPA axis in depression.
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PMID:Gene expression analysis in the human hypothalamus in depression by laser microdissection and real-time PCR: the presence of multiple receptor imbalances. 1860 75

The hormonal control of cell death is currently the best-established mechanism for creating sex differences in cell number in the brain and spinal cord. For example, males have more cells than do females in the principal nucleus of the bed nucleus of the stria terminalis (BNSTp) and spinal nucleus of the bulbocavernosus (SNB), whereas females have a cell number advantage in the anteroventral periventricular nucleus (AVPV). In each case, the difference in cell number in adulthood correlates with a sex difference in the number of dying cells at some point in development. Mice with over- or under-expression of cell death genes have been used to test more directly the contribution of cell death to neural sex differences, to identify molecular mechanisms involved, and to determine the behavioural consequences of suppressing developmental cell death. Bax is a pro-death gene of the Bcl-2 family that is singularly important for apoptosis in neural development. In mice lacking bax, the number of cells in the BNSTp, SNB and AVPV are significantly increased, and sex differences in total cell number in each of these regions are eliminated. Cells rescued by bax gene deletion in the BNSTp express markers of differentiated neurones and the androgen receptor. On the other hand, sex differences in other phenotypically identified populations, such as vasopressin-expressing neurones in the BNSTp or dopaminergic neurones in AVPV, are not affected by either bax deletion or bcl-2 over-expression. Possible mechanisms by which testosterone may regulate cell death in the nervous system are discussed, as are the behavioural effects of eliminating sex differences in neuronal cell number.
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PMID:Control of cell number in the sexually dimorphic brain and spinal cord. 1920 22

In most vertebrate species, the production of vasotocin (VT; non-mammals) and vasopressin (VP; mammals) in the medial bed nucleus of the stria terminalis (BSTm) waxes and wanes with seasonal reproductive state; however, opportunistically breeding species might need to maintain high levels of this behaviorally relevant neuropeptide year-round in anticipation of unpredictable breeding opportunities. We here provide support for this hypothesis and demonstrate that these neurons are instead regulated 'cryptically' via hormonal regulation of their activity levels, which may be rapidly modified to adjust VT signaling. First, we show that combined treatment of male and female zebra finches (Estrildidae: Taeniopygia guttata) with the androgen receptor antagonist flutamide and the aromatase inhibitor 1,4,6-androstatriene-3,17-dione does not alter the expression of VT immunoreactivity within the BSTm; however, both hormonal treatment and social housing environment (same-sex versus mixed-sex) alter VT colocalization with the immediate early gene product Fos (a proxy marker of neural activation) in the BSTm. In a second experiment, manipulations of estradiol (E2) levels with the aromatase inhibitor letrozole (LET) or subcutaneous E2 implants failed to alter colocalization, suggesting that the colocalization effects in experiment 1 were solely androgenic. LET treatment also did not affect VT immunoreactivity in a manner reversible by E2 treatment. Finally, comparisons of VT immunoreactivity in breeding and nonbreeding individuals of several estrildid species demonstrate that year-round stability of VT immunoreactivity is found only in highly opportunistic species, and is therefore not essential to the maintenance of long-term pair bonds, which are ubiquitous in the Estrildidae.
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PMID:Cryptic regulation of vasotocin neuronal activity but not anatomy by sex steroids and social stimuli in opportunistic desert finches. 2033 15


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