B Receptor (b + receptor)

Distribution by Scientific Domains


Selected Abstracts


Functional immunohistochemistry of neuropeptides and nitric oxide synthase in the nerve fibers of the supratentorial dura mater in an experimental migraine model

MICROSCOPY RESEARCH AND TECHNIQUE, Issue 3 2001
Elizabeth Knyihár-Csillik
Abstract The supratentorial cerebral dura of the albino rat is equipped with a rich sensory innervation both in the connective tissue and around blood vessels, which includes nociceptive axons and their terminals; these display intense calcitonin gene-related peptide (CGRP) immunoreactivity. Stereotactic electrical stimulation of the trigeminal (Gasserian) ganglion, regarded as an experimental migraine model, caused marked increase and disintegration of club-like perivascular CGRP-immunopositive nerve endings in the dura mater and induced an apparent increase in the lengths of CGRP-immunoreactive axons. Intravenous administration of sumatriptan or eletriptan, prior to electrical stimulation, prevented disintegration of perivascular terminals and induced accumulation of CGRP in terminal and preterminal portions of peripheral sensory axons. Consequently, immunopositive terminals and varicosities increased in size; accumulation of axoplasmic organelles resulted in the "hollow" appearence of numerous varicosities. Since triptans exert their anti-migraine effect by virtue of agonist action on 5-HT1D/B receptors, we suggest that these drugs prevent the release of CGRP from perivascular nerve terminals in the dura mater by an action at 5-HT1D/B receptors. Nitroglycerine (NitroPOHL), given subcutaneously to rats, induces increased beading of nitric oxide synthase (NOS)-immunoreactive nerve fibers in the supratentorial cerebral dura mater, and an apparent increase in the number of NOS-immunoreactive nerve fibers in the dural areas supplied by the anterior and middle meningeal arteries, and the sinus sagittalis superior. Structural alterations of nitroxidergic axons innervating blood vessels of the dura mater support the idea that nitric oxide (NO) is involved in the induction of headache, a well-known side effect of coronary dilator agents. Microsc. Res. Tech. 53:193,211, 2001. © 2001 Wiley-Liss, Inc. [source]


Spasmogenic action of endothelin-1 on isolated equine pulmonary artery and bronchus

EQUINE VETERINARY JOURNAL, Issue 2 2003
A. E. M. BENAMOU
Summary Reasons for performing study: There is currently little published information about the effects of endothelin-1 (ET-1), a potent endogenous spasmogen of vascular and airway smooth muscle, on pulmonary vasculature and airways or which ET receptor subtypes mediate ET-1-induced vasoconstrictive and bronchoconstrictive action in the horse. Objectives: To investigate the effect of endothelin-1 (ET-1) on smooth muscle from isolated equine pulmonary artery and bronchus. In addition, the roles of ETA and ETB receptors in ET-1 mediated contraction in these tissues were assessed. Methods: The force generation of ring segments from pulmonary arteries or third-generation airways (obtained from horses subjected to euthanasia fororthopaedic reasons) were studied in an organ bath at 37°C in response to exogenous endothelin and selective endothelin A (BQ123) or B receptor (BQ788) antagonists. Results: ET-1 produced concentration-dependent contractions of the equine pulmonary artery and bronchus. The threshold for contraction was 10,10 and 10,9 mol/l ET-1 for pulmonary artery and bronchus, respectively. The maximal contraction induced by the highest ET-1 concentration (10,7 mol/l) was 173 and 194% of the contraction obtained with 100 mmol/l KCl in pulmonary artery and bronchus, respectively. ET-1 potency was 25 times greater in equine pulmonary artery than in equine bronchus (concentration of ET-1 producing 50% of maximal contraction [EC50] = 5.6 10,9 mol/l and 2.2 10,8 mol/l, respectively). In pulmonary artery, ET-1 induced contractions were significantly inhibited by the ETA receptor antagonist BQ123 (1 ,mol/l; dose-response curve to ET-1 was shifted to the right by 5.4-fold), but not by the ETB antagonist BQ788. In bronchus, dose-responses curves to ET-1 were shifted to the right by BQ123 (1 ,mol/l; 2.5-fold), but not by BQ788 (1 ,mol/l). In the presence of both antagonists, the dose-response curve to ET-1 was shifted to the right by 4.5-fold. Conclusions: These functional studies demonstrate that ET-1 is a potent spasmogen of equine third generation pulmonary artery and bronchus, and that contractions are mediated via ETA receptors in the former and both ETA and ETB receptors in the latter. Potential clinical relevance: Endothelin receptor antagonists may have potential for treating equine pulmonary hypertension or bronchoconstriction. [source]


Brain-derived neurotrophic factor induces long-lasting Ca2+ -activated K+ currents in rat visual cortex neurons

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2002
Yoshito Mizoguchi
Abstract Brain-derived neurotrophic factor (BDNF) increases postsynaptic intracellular Ca2+ and modulates synaptic transmission in various types of neurons. Ca2+ -activated K+ currents, opened mainly by intracellular Ca2+ elevation, contribute to hyperpolarization following action potentials and modulate synaptic transmission. We asked whether BDNF induces Ca2+ -activated K+ currents by postsynaptic elevation of intracellular Ca2+ in acutely dissociated visual cortex neurons of rats. Currents were analysed using the nystatin-perforated patch clamp technique and imaging of intracellular Ca2+ mobilization with fura-2. At a holding potential of ,50 mV, BDNF application (20 ng/mL) for 1,2 min induced an outward current (IBDNF-OUT; 80.0 ± 29.0 pA) lasting for more than 90 min without attenuation in every neuron tested. K252a (200 nm), an inhibitor of Trk receptor tyrosine kinase, and U73122 (3 ,m), a specific phospholipase C (PLC)-, inhibitor, suppressed IBDNF-OUT completely. IBDNF-OUT was both charybdotoxin- (600 nm) and apamin- (300 nm) sensitive, suggesting that this current was carried by Ca2+ -activated K+ channels. BAPTA-AM (150 ,m) gradually suppressed IBDNF-OUT. Fura-2 imaging revealed that a brief application of BDNF elicited a long-lasting elevation of intracellular Ca2+. These results show that BDNF induces long-lasting Ca2+ -activated K+ currents by sustained intracellular Ca2+ elevation in rat visual cortex neurons. While BDNF, likely acting through the Trk B receptor, was necessary for the induction of long-lasting Ca2+ -activated K+ currents via intracellular Ca2+ elevation, BDNF was not necessary for the maintenance of this current. [source]


Disruption of the gene encoding 3,-hydroxysterol ,14 -reductase (Tm7sf2) in mice does not impair cholesterol biosynthesis

FEBS JOURNAL, Issue 20 2008
Anna M. Bennati
Tm7sf2 gene encodes 3,-hydroxysterol ,14 -reductase (C14SR, DHCR14), an endoplasmic reticulum enzyme acting on ,14 -unsaturated sterol intermediates during the conversion of lanosterol to cholesterol. The C-terminal domain of lamin B receptor, a protein of the inner nuclear membrane mainly involved in heterochromatin organization, also possesses sterol ,14 -reductase activity. The subcellular localization suggests a primary role of C14SR in cholesterol biosynthesis. To investigate the role of C14SR and lamin B receptor as 3,-hydroxysterol ,14 -reductases, Tm7sf2 knockout mice were generated and their biochemical characterization was performed. No Tm7sf2 mRNA was detected in the liver of knockout mice. Neither C14SR protein nor 3,-hydroxysterol ,14 -reductase activity were detectable in liver microsomes of Tm7sf2(,/,) mice, confirming the effectiveness of gene inactivation. C14SR protein and its enzymatic activity were about half of control levels in the liver of heterozygous mice. Normal cholesterol levels in liver membranes and in plasma indicated that, despite the lack of C14SR, Tm7sf2(,/,) mice are able to perform cholesterol biosynthesis. Lamin B receptor 3,-hydroxysterol ,14 -reductase activity determined in liver nuclei showed comparable values in wild-type and knockout mice. These results suggest that lamin B receptor, although residing in nuclear membranes, may contribute to cholesterol biosynthesis in Tm7sf2(,/,) mice. Affymetrix microarray analysis of gene expression revealed that several genes involved in cell-cycle progression are downregulated in the liver of Tm7sf2(,/,) mice, whereas genes involved in xenobiotic metabolism are upregulated. [source]


The role of endothelin-1 and the endothelin B receptor in the pathogenesis of hepatopulmonary syndrome in the rat

HEPATOLOGY, Issue 6 2004
Yiqun Ling
Endothelin-1 (ET-1) stimulation of endothelial nitric oxide synthase (eNOS) via pulmonary endothelial endothelin B (ETB) receptors and pulmonary intravascular macrophage accumulation with expression of inducible nitric oxide synthase (iNOS) and heme oxygenase-1 (HO-1) are implicated in experimental hepatopulmonary syndrome (HPS) after common bile duct ligation (CBDL). Our aim was to evaluate the role of ET-1 in the development of experimental HPS. The time course of molecular and physiological changes of HPS and the effects of selective endothelin receptor antagonists in vivo were assessed after CBDL. Effects of ET-1 on intralobar pulmonary vascular segment reactivity and on eNOS expression and activity in rat pulmonary microvascular endothelial cells (RPMVECs) were also evaluated. Hepatic and plasma ET-1 levels increased 1 week after CBDL in association with a subsequent increase in pulmonary microvascular eNOS and ETB receptor levels and the onset of HPS. Selective ETB receptor inhibition in vivo significantly decreased pulmonary eNOS and ETB receptor levels and ameliorated HPS. CBDL pulmonary artery segments had markedly increased ETB receptor mediated, nitric oxide dependent vasodilatory responses to ET-1 compared with controls and ET-1 triggered an ETB receptor dependent stimulation of eNOS in RPMVECs. Pulmonary intravascular macrophages also accumulated after CBDL and expressed HO-1 and iNOS at 3 weeks. Selective ETB receptor blockade also decreased macrophage accumulation and iNOS production. In conclusion, ET-1 plays a central role in modulating pulmonary micovascular tone in experimental HPS. (HEPATOLOGY 2004;39:1593,1602.) [source]


ABCD syndrome is caused by a homozygous mutation in the EDNRB gene

AMERICAN JOURNAL OF MEDICAL GENETICS, Issue 3 2002
Joke B.G.M. Verheij
Abstract ABCD syndrome is an autosomal recessive syndrome characterized by albinism, black lock, cell migration disorder of the neurocytes of the gut (Hirschsprung disease [HSCR]), and deafness. This phenotype clearly overlaps with the features of the Shah-Waardenburg syndrome, comprising sensorineural deafness; hypopigmentation of skin, hair, and irides; and HSCR. Therefore, we screened DNA of the index patient of the ABCD syndrome family for mutations in the endothelin B receptor (EDNRB) gene, a gene known to be involved in Shah-Waardenburg syndrome. A homozygous nonsense mutation in exon 3 (R201X) of the EDNRB gene was found. We therefore suggest that ABCD syndrome is not a separate entity, but an expression of Shah-Waardenburg syndrome. © 2002 Wiley-Liss, Inc. [source]


Reduced endothelin-3 expression in sporadic Hirschsprung disease

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 5 2000
S. E. Kenny
Background: Enteric aganglionosis in Hirschsprung disease has been linked to genes coding for endothelin-3 (EDN3) and the endothelin B receptor (EDNRB), but there is no such linkage in most patients with sporadic Hirschsprung disease. However, the similarity between the distal colonic aganglionosis in Hirschsprung disease and that due to EDN3 or EDNRB mutations led to the hypothesis that levels of expression of these genes might be affected in the absence of mutation, thus causing the Hirschsprung disease phenotype. The aim of this study was to determine EDN3 and EDNRB messenger RNA (mRNA) levels in tissue samples from patients with sporadic Hirschsprung disease. Methods: RNA and DNA were isolated from the ganglionic and aganglionic colonic segments of ten children with sporadic Hirschsprung disease, and from the colon of ten age-matched controls. The DNA was analysed for mutations in the genes coding for endothelin-3 (ET-3) and endothelin B receptor (ET-B) proteins. Relative levels of EDN3 and EDNRB mRNA were determined by semi-quantitative transcriptase,polymerase chain reaction. Results: Three children had sequence variants in EDN3 and EDNRB. In the remaining seven patients, EDN3 mRNA levels were reduced in both the ganglionic and aganglionic colon compared with levels in controls; there was no difference in expression of EDNRB between groups. Conclusion: In the absence of mutation, EDN3 is downregulated in short-segment Hirschsprung disease, suggesting that this may be a common step leading to aganglionosis. © 2000 British Journal of Surgery Society Ltd [source]


Detection of tumor specific gene expression in bone marrow and peripheral blood from patients with small cell lung carcinoma

CANCER, Issue 4 2003
Masato Shingyoji M.D.
Abstract BACKGROUND Small cell lung carcinoma (SCLC) has the propensity to grow rapidly and metastasize extensively. Detection of micro-dissemination of SCLC may have clinical relevance. For its detection, tumor-specific gene expressions were examined in peripheral blood and bone marrow aspirate from patients with SCLC. METHODS Expression of prepro-gastrin-releasing peptide (preproGRP), neuromedin B receptor (NMB-R) and gastrin-releasing peptide receptor (GRP-R) were examined by reverse transcriptase polymerase chain reaction (RT-PCR) in peripheral blood and bone marrow aspirate from 40 untreated patients with SCLC. Control samples consisted of peripheral blood samples from 5 patients with nonsmall cell lung cancer (NSCLC) and 20 healthy volunteers. RESULTS Positive rates of preproGRP, NMB-R, and GRP-R in bone marrow aspirate of patients with SCLC were 23% (9/40), 8% (3/40), and 10% (4/40), respectively. Those rates in peripheral blood were 11% (4/38), 5% (2/38), and 29% (11/38), respectively. Although GRP-R expression was detected in patients with NSCLC and in healthy volunteers, preproGRP and NMB-R expressions were not detected in patients with NSCLC and in healthy volunteers. All three gene expressions in bone marrow were more frequently observed in patients with bone marrow metastasis, accessed by biopsy, than in patients without. PreproGRP gene expression in bone marrow was also more frequent in patients with bone metastasis, accessed by bone scintigram, than in patients without, and was related to poorer survival. CONCLUSIONS Micro-dissemination of SCLC was detectable by RT-PCR of preproGRP and NMB-R, both specific for SCLC. These gene expressions in bone marrow may be related to disease extent and prognosis. Cancer 2003;97:1057,62. © 2003 American Cancer Society. DOI 10.1002/cncr.11108 [source]


Hair interior defect in AKR/J mice

CLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 4 2009
K. A. Giehl
Summary Background., All AKR/J mice have a subtle defect that involves malformation of the central portion of hair fibres that is best visualized under white and polarized light microscopy. Aims., This study sought to characterize the clinical and ultrastructural features of the hair interior defect (HID) phenotype and to determine the chromosomal localization of the hid mutant gene locus. Methods., White and polarized light microscopy combined with scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were used to characterize the HID phenotype. Complementation testing and gene-linkage studies were performed to map the locus. Results., Using SEM, the hair-fibre structure on the surface was found to be similar to hairs obtained from normal BALB/cByJ+/+and C57BL/6 J+/+mice. There were also no differences in sulphur content. TEM revealed degenerative changes in the medulla similar to that seen by light microscopy. This autosomal recessive mutation is called HID (locus symbol: hid). We mapped the hid locus to the distal end of mouse chromosome 1. No genes reported to cause skin or hair abnormalities are known to be within this interval except for the lamin B receptor (Lbr), which had been excluded previously as the cause of the hid phenotype in AKR/J mice. Conclusion., A potentially novel gene or known gene with a novel phenotype resides within this interval, which may shed light on human diseases with defects in the inner structure of the hair fibre. [source]


, -Amino Butyric Acid Control of Arginine Vasopressin Release from the Ewe Hypothalamus In Vitro: Sensitivity to Oestradiol

REPRODUCTION IN DOMESTIC ANIMALS, Issue 5 2007
SPS Ghuman
Contents The present study aims to ascertain the influence of , -amino butyric acid (GABA)A or B receptors on arginine vasopressin (AVP) release in vitro and determine whether E2 modulates GABA,AVP interaction. Within 10 min of ewe killing, saggital midline hypothalamic slices (from the anterior preoptic area to the mediobasal hypothalamus along with the median eminence, 2-mm thick, two per ewe) were dissected, placed in oxygenated minimum essential media (MEM)- , at 4°C and within 2 h were singly perifused at 37°C with oxygenated MEM- , (pH 7.4; flow rate 0.15 ml/min), either with or without E2 (24 pg/ml). After 4-h equilibration, 10-min fractions were collected for 4 h interposed with a 10-min exposure at 60 min to a specific GABAA or B receptor agonist or antagonist at various doses (0.1,10 mm). GABAA (muscimol; no E2, n = 7 perifusion chambers, with E2, n = 11) or GABAB (baclofen; no E2, n = 8, with E2, n = 15) agonists (10 mm) did not influence AVP concentrations. However, AVP release increased (p < 0.05) 20,30 min after exposure to 10 mm GABAA or B antagonists (bicuculline, no E2, n = 7: from 4.6 ± 0.7 to 33.0 ± 0.4, with E2, n = 17: from 11.9 ± 1.4 to 32.8 ± 6.0; CGP52432, with E2, n = 14: from 14.0 ± 2.6 to 28.8 ± 3.9 pg/ml). At the end of the collection period, hypothalamic slices responded to KCl (100 mm) with AVP efflux (p < 0.05). GABAB but not GABAA antagonist-stimulated AVP release was enhanced in the presence of E2. In summary, AVP release is under the inhibitory influence of GABA input with further potentiation by E2 through GABAB receptors in vitro. [source]


Close linkage of genes encoding receptors for subgroups A and C of avian sarcoma/leucosis virus on chicken chromosome 28

ANIMAL GENETICS, Issue 3 2004
D. Elleder
Summary Avian sarcoma and leucosis viruses (ASLV) are classified into six major subgroups (A to E and J) according to the properties of the viral envelope proteins and the usage of cellular receptors for virus entry. Subgroup A and B receptors are identified molecularly and their genomic positions TVA and TVB are mapped. The subgroup C receptor is unknown, its genomic locus TVC is reported to be genetically linked to TVA, which resides on chicken chromosome 28. In this study, we used two chicken inbred lines that carry different alleles coding for resistance (TVCR) and sensitivity (TVCS) to infection by subgroup C viruses. A backross population of these lines was tested for susceptibility to subgroup C infection and genotyped for markers from chicken chromosome 28. We confirmed the close linkage between TVA and TVC loci. Further, we have described the position of TVC on chromosome 28 relative to markers from the consensus map of the chicken genome. [source]