Role of endothelin receptor subtype B(ET-B) in myocardial ischemia

Life Sciences ◽  
1994 ◽  
Vol 55 (23) ◽  
pp. 1833-1844 ◽  
Author(s):  
Carol A. Sargent ◽  
Eddie C.K. Liu ◽  
Chia-ching Chao ◽  
Maria L. Webb ◽  
Gary J. Grover
Keyword(s):  
Myocardial Ischemia ◽  
Receptor Subtype ◽  
Endothelin Receptor ◽  
Subtype B

Role of endothelin-1 in neointima formation after endothelial removal in rabbit carotid arteries

1994 ◽  
Vol 267 (6) ◽  
pp. H2259-H2267 ◽  
Author(s):  
H. Azuma ◽  
H. Hamasaki ◽  
Y. Niimi ◽  
T. Terada ◽  
O. Matsubara
Keyword(s):  
Time Course ◽  
Plasma Concentrations ◽  
Tissue Level ◽  
Nuclear Antigen ◽  
Control Group ◽  
Receptor Subtype ◽  
Neointima Formation ◽  
Subtype B ◽  
Selective Ligand

To investigate the role of local endothelin (ET)-1 in neointima formation, we performed a balloon denudation in the rabbit carotid artery. Four weeks after denudation, regeneration of endothelial cells was almost complete, and a marked intimal hyperplasia was observed. The tissue level of ET-1-like immunoreactivity was significantly increased even at 24 and 72 h after denudation and was 9.3 times higher than the control group in 4 wk. On the same time course, the proliferating cell nuclear antigen (PCNA)-positive cells clearly appeared. Receptor density values for 125I-ET-1 and 125I-IRL-1620 [ET-receptor subtype B (ETB)-selective ligand] bindings were significantly greater in the hyperplastic artery without changes in dissociation equilibrium constant values. The 125I-ET-1 binding sites not inhibited with BQ-123 [ET-receptor subtype A (ETA)-selective antagonist] were significantly increased in hyperplastic arteries. ETB receptors were more densely localized in the neointima. The chronic intravenous administration of BQ-123 at plasma concentrations sufficient to antagonize the ETA receptors had no effect on neointima formation and the appearance of PCNA-positive cells. We concluded from all results that ET-1 would be involved in neointima formation after endothelial removal and that the ETA receptors would not play a role in this process.

scholarly journals Endothelin Receptor Subtype B Mediates Autoinduction of Endothelin-1 in Rat Mesangial Cells

1995 ◽  
Vol 270 (12) ◽  
pp. 6997-7003 ◽  
Author(s):  
Shigeki Iwasaki ◽  
Toshio Homma ◽  
Yuzuru Matsuda ◽  
Valentina Kon
Keyword(s):  
Mesangial Cells ◽  
Receptor Subtype ◽  
Endothelin Receptor ◽  
Endothelin 1 ◽  
Subtype B

Polymorphisms of EDNRB, ATG, and ACE genes in salt-sensitive hypertensionThis article is one of a selection of papers published in the special issue (part 2 of 2) on Forefronts in Endothelin.

2008 ◽  
Vol 86 (8) ◽  
pp. 505-510 ◽  
Author(s):  
Jessica Caprioli ◽  
Caterina Mele ◽  
Chiara Mossali ◽  
Laura Gallizioli ◽  
Gilberta Giacchetti ◽  
...  
Keyword(s):  
Protective Role ◽  
Receptor Subtype ◽  
Genotype Distribution ◽  
High Salt Diet ◽  
Subtype B ◽  
Salt Depletion ◽  
Sensitivity Data ◽  
Pressure Changes ◽  
Salt Sensitive Hypertension

Almost 50% of hypertensive individuals manifest blood pressure changes in response to salt depletion or repletion and are termed “salt sensitive” (SS). Blunted activity of the endothelin (ET) system and the renin–angiotensin–aldosterone system (RAAS) have been reported as possible mechanisms contributing to salt sensitivity. Data are available that endothelin receptor subtype B (ETBR)-deficient rats develop salt-sensitive hypertension when fed a high-salt diet. Whether the ETBR gene (EDNRB) is involved in genetic predisposition to human salt-sensitive hypertension has not been studied so far. We screened EDNRB in 104 hypertensive patients (49 salt sensitive and 55 salt resistant) and 110 normotensive controls. No new sequence variation was found, but genotype distribution of the common polymorphism G1065A revealed that the AA + GA genotypes were significantly more frequent in salt-resistant than in salt-sensitive individuals (p = 0.007), suggesting a protective role for the A allele. We also screened angiotensinogen gene AGT M235T and angiotensin-converting enzyme insertion/deletion polymorphism ACE I/D and found an association between TT genotype and hypertension. A possible synergistic effect to salt-sensitive hypertension was found by combining EDNRB GG with ACE DD/ID genotypes. In conclusion, our data confirm the role of ET system and RAAS in salt-sensitive hypertension.

W276 Mutation in the Endothelin Receptor Subtype B Impairs GqCoupling but Not Gior GoCoupling†

Biochemistry ◽  
2000 ◽  
Vol 39 (4) ◽  
pp. 686-692 ◽  
Author(s):  
Fumiaki Imamura ◽  
Ikuyo Arimoto ◽  
Yoshinori Fujiyoshi ◽  
Tomoko Doi
Keyword(s):  
Receptor Subtype ◽  
Endothelin Receptor ◽  
Subtype B

scholarly journals Production and binding of endothelin-2 (EDN2) in the rat ovary: endothelin receptor subtype A (EDNRA)-mediated contraction

2010 ◽  
Vol 22 (5) ◽  
pp. 780 ◽  
Author(s):  
Phillip J. Bridges ◽  
Misung Jo ◽  
Linah Al Alem ◽  
Giyoun Na ◽  
Wen Su ◽  
...  
Keyword(s):  
Follicular Development ◽  
Isometric Tension ◽  
Receptor Subtype ◽  
Endothelin Receptor ◽  
Synergistic Interactions ◽  
Endothelin Receptor A ◽  
Rat Ovary ◽  
Subtype A ◽  
Tension Analysis

Endothelin-2 (EDN2)-mediated contraction has been proposed as a final mechanical signal facilitating ovulation. The objectives herein were to determine (1) whether ovarian endothelins were increased before ovulation; (2) whether a specific endothelin-converting enzyme (ECE) was mediating their production; (3) which receptor was facilitating ovarian contraction; and (4) whether receptor-specific antagonism affected ovulation. Follicular development was induced in immature rats with 10 IU pregnant mare serum gonadotrophin (PMSG) and the ovulatory cascade was initiated 48 h later with 10 IU human chorionic gonadotrophin (hCG). In Experiment 1, an immunoassay revealed that the ovarian concentration of endothelin peptide was increased 7-fold 12 h after hCG when compared with 48 h after PMSG (P < 0.05). In Experiment 2, real-time PCR indicated that mRNA for Ece1, but not Ece2, was increased in granulosa cells collected 12 h after hCG when compared with those collected before the ovulatory stimulus (P < 0.05). In Experiment 3, isometric tension analysis revealed that the contractile effect of EDN2 was mediated by endothelin receptor A (EDNRA), not B (EDNRB). In Experiment 4, no effect was observed on the rate of ovulation when rats were treated with an antagonist specific to EDNRA (BQ123) or EDNRB (BQ788), or when mice were treated with BQ123, BQ788 or BQ123 + BQ788. In conclusion, endothelin peptide is produced before ovulation and the contractile action of EDN2 within the ovary is facilitated via EDNRA. In addition, findings of this study indicate synergistic interactions among contractile factors affect ovulatory outcome, while the role of EDNRB alone in the process of ovulation requires further investigation.

Identification and Characterization of Endothelin Receptor Subtype B in Rat Retina

1993 ◽  
Vol 61 (3) ◽  
pp. 1113-1119 ◽  
Author(s):  
J. A. Juan ◽  
F. J. Moya ◽  
M. Garcia de Lacoba ◽  
A. Fernandez-Cruz ◽  
R. Fernandez-Durango
Keyword(s):  
Receptor Subtype ◽  
Endothelin Receptor ◽  
Rat Retina ◽  
Subtype B ◽  
Identification And Characterization

Endothelin-1 plays a major role in portal hypertension of biliary cirrhotic rats through endothelin receptor subtype B together with subtype A in vivo

2001 ◽  
Vol 34 (6) ◽  
pp. 805-811 ◽  
Author(s):  
Hideyuki Kojima ◽  
Shinya Sakurai ◽  
Shigeki Kuriyama ◽  
Hitoshi Yoshiji ◽  
Hiroo Imazu ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Receptor Subtype ◽  
Endothelin Receptor ◽  
Endothelin 1 ◽  
Subtype B ◽  
Subtype A

Downregulation of endothelin receptors by autocrine production of endothelin-1

1993 ◽  
Vol 265 (1) ◽  
pp. C188-C192 ◽  
Author(s):  
M. Clozel ◽  
B. M. Loffler ◽  
V. Breu ◽  
L. Hilfiger ◽  
J. P. Maire ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Mesangial Cells ◽  
Binding Capacity ◽  
Umbilical Vein ◽  
Receptor Subtype ◽  
Endothelin Receptor ◽  
Endothelin 1 ◽  
Subtype B ◽  
Maximal Binding ◽  
Umbilical Vein Endothelial Cells

The potent vasoconstrictor endothelin-1 (ET-1) is a paracrine, but also autocrine, factor for some types of cells. The goal of our study was to evaluate whether the receptor population in cells expressing endothelin receptor subtype A (rat mesangial cells) or endothelin receptor subtype B (human and rat endothelial cells) was affected by the autocrine production of ET-1. We therefore studied maximal binding capacity of 125I-labeled ET-1 in the presence or absence of the metalloprotease inhibitors phosphoramidon, which blocks the intracellular processing of Big ET-1 to ET-1, and thiorphan, which does not block this conversion. Phosphoramidon inhibited the release of ET-1 by human umbilical vein endothelial cells, rat aortic endothelial cells, and rat mesangial cells, and increased 1.4- to 17-fold the maximal binding capacity in the three types of cells. Thiorphan affected neither ET-1 release nor binding. The increase in receptor binding by phosphoramidon was associated with an increase in the functional effect of ET-1, as measured by arachidonic acid release in rat mesangial cells. We conclude that autocrine production of ET-1 decreases, either by binding or by downregulation, the number of binding sites available for ET-1 of paracrine or systemic sources. This aspect of modulation of the vasoconstrictor effect of endothelin should be considered in pathological situations or after endothelin-converting-enzyme inhibition.

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