The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Gene Review

EDNRB  -  endothelin receptor type B

Sus scrofa

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of ETB

  • These studies were designed to test the hypothesis that experimental hypercholesterolemia is characterized by a differentially altered coronary contractile response to ETA- and ETB-receptor stimulation, in vitro [1].
  • The amino acid sequences of these four toxins were homologous to the earlier described exfoliative toxins SHETB from S. hyicus and ETA, ETB, and ETD from Staphylococcus aureus [2].
  • Taken together, our present observations suggest that ET(s) influences pulmonary functions by constricting airway smooth muscle via ETB receptors during the immediate asthmatic response and by modulating pulmonary inflammation via ETA receptors during the late asthmatic response, respectively [3].
  • Plasma ET-1 increased from 1.50 and 1.17 ng/L at baseline to 2.07 and 3.18 ng/L at the end of hypoxemia in the ETA and ETB groups respectively [4].
  • The vasoconstriction induced by the ETB receptor agonist [Ala 1,3,11,15] ET-1 or serotonin was not significantly affected by ischemia/reperfusion [5].

High impact information on ETB

  • Two endothelin receptors (ETA and ETB) expressed on circular smooth muscle cells of guinea pig cecum [6].
  • CONCLUSIONS: The results show a direct contractile effect of ETs on circular smooth muscle of guinea pig cecum and the presence of both ETA- and ETB-receptor subtypes [6].
  • Endothelin-1 (ET-1) is a 21-amino acid peptide hormone released from myocardial and endothelial cells, whose receptors (both ETA and ETB are expressed in the myocardium [7].
  • The effect of ET-1 appeared to be mediated by an ETA receptor, because it was prevented by FR139317, an ETA-selective antagonist (1 mumol/L, n = 4), and sarafotoxin s6c, an ETB-selective agonist (100 nmol/L, n = 4), could not inhibit the ISO-enhanced IK [7].
  • These studies demonstrate that experimental hypercholesterolemia is characterized by enhanced coronary vasoconstriction to endothelins in vitro, the mechanism of which is mediated mainly through the ETB receptor [1].

Chemical compound and disease context of ETB


Biological context of ETB

  • Studies were conducted to determine whether endothelin (ET) ETA and ETB receptor protein and mRNA expression is developmentally regulated in the postnatal swine mesenteric circulation [10].
  • This finding combined with the observed relative potencies of the peptides (IRL 1620 > ET-1 = ET-3) suggests that pulmonary vasodilatation was mediated by activation of the non-selective ETB receptor [11].
  • In vitro constrictive responses of isolated tracheas and bronchi to ET1 were inhibited mainly by BQ123 and BQ788, respectively, which suggested that distribution of ETA and ETB receptors for bronchoconstriction are topographically distinct along airways [3].
  • The binding affinity of LLC-PK1 cells was about 10,000 times higher for the ETB antagonist BQ-788 [N-cis-2,6-dimethyl-piperidinocarbonyl-L-tau-metylleucyl-D-+ ++Nin- methoxycarbonyltryptophanyl-D-norleucine] (IC50, 1.3 nM) than for the ETA antagonist BQ-123 [cyclo-(D-Trp-D-Asp-Pro-D-Val-Leu)] (IC50, 14 microM) [12].
  • Direct activation of ETA expressed on the basal cells caused enhancement of their growth, whereas that of ETB expressed on the ciliated columnar cells caused suppression of the basal cell growth [13].

Anatomical context of ETB

  • Thus, the ETB receptor has a role in regulation of coronary artery tone in both the steady-state and pathophysiological states [1].
  • Influence of regional differences in ETA and ETB receptor subtype proportions on endothelin-1-induced contractions in porcine isolated trachea and bronchus [14].
  • These experiments indicated the presence of functioning ETA receptors in addition to ETB receptors in endothelial cells in situ [15].
  • Therefore, the ETB receptors in LLC-PK1 cells couple to the two types of signal transduction cascades to reduce cAMP production and stimulate cGMP production via distinct G-proteins [12].
  • Furthermore, blockade of either ETA or ETB compromised the epithelial cell layer formation under the air-interphase culture, which indicates the dependence of tracheal epithelial remodeling on a balance between the positive and negative effects of ET-1 on the basal cell growth [13].

Associations of ETB with chemical compounds

  • The coronary vasoconstrictor effects of endothelins, mediated by both endothelin ETA and ETB receptors, may be differentially altered in pathophysiological states associated with endothelial dysfunction and elevated endothelin levels [1].
  • Incubation of arteries from hypercholesterolemic pigs with BQ-788 (ETB-receptor antagonist), but not FR-139317 (ETA-receptor antagonist), altered the contractile response to ET-1 at 10(-10) mol/L [1].
  • The ETB selective antagonist BQ-788 (100 nM) shifted S6c responses rightward but produced no change in ET-1 responses [16].
  • 4. In trachea, endothelin-1 induced contractions were not significantly inhibited by either the ETA receptor-selective antagonist, BQ-123 (3 microM) or the ETB receptor-selective antagonist, BQ-788 (1 microM) [14].
  • 3. In the same perfused model, the selective ETB agonist, IRL 1620 (50 nM), stimulated the release of thromboxane A2, but not prostacyclin [17].

Other interactions of ETB

  • Losartan therapy was associated with persistent overexpressions of ANG II, AT2, ET-1, ETB, and angiopoietin-1 and with a return to normal of the BMPR-2 expression [18].
  • We conclude that ETB receptors play a central role in mediating ET-1-induced vasoconstriction in pig skin, and the mechanism probably involves L-type Ca2+ channels, PLC, and PKC [19].

Analytical, diagnostic and therapeutic context of ETB


  1. Enhanced endothelin-B-receptor-mediated vasoconstriction of small porcine coronary arteries in diet-induced hypercholesterolemia. Hasdai, D., Mathew, V., Schwartz, R.S., Smith, L.A., Holmes, D.R., Katusic, Z.S., Lerman, A. Arterioscler. Thromb. Vasc. Biol. (1997) [Pubmed]
  2. Cloning and sequence analysis of genes encoding Staphylococcus hyicus exfoliative toxin types A, B, C, and D. Ahrens, P., Andresen, L.O. J. Bacteriol. (2004) [Pubmed]
  3. Involvement of endothelins in immediate and late asthmatic responses of guinea pigs. Uchida, Y., Jun, T., Ninomiya, H., Ohse, H., Hasegawa, S., Nomura, A., Sakamoto, T., Sardessai, M.S., Hirata, F. J. Pharmacol. Exp. Ther. (1996) [Pubmed]
  4. Effects of selective inhibition of the endothelin A and B receptors on hypoxic pulmonary vasoconstriction in newborn piglets. Medbø, S., Frøen, J.F., Saugstad, O.D. Journal of perinatal medicine. (2001) [Pubmed]
  5. Myocardial release of endothelin (ET) and enhanced ET(A) receptor-mediated coronary vasoconstriction after coronary thrombosis and thrombolysis in pigs. Wang, Q.D., Uriuda, Y., Pernow, J., Hemsén, A., Sjöquist, P.O., Rydén, L. J. Cardiovasc. Pharmacol. (1995) [Pubmed]
  6. Two endothelin receptors (ETA and ETB) expressed on circular smooth muscle cells of guinea pig cecum. Okabe, H., Chijiiwa, Y., Nakamura, K., Yoshinaga, M., Akiho, H., Harada, N., Nawata, H. Gastroenterology (1995) [Pubmed]
  7. Endothelin-1 inhibits the slow component of cardiac delayed rectifier K+ currents via a pertussis toxin-sensitive mechanism. Washizuka, T., Horie, M., Watanuki, M., Sasayama, S. Circ. Res. (1997) [Pubmed]
  8. Hypoxic pulmonary endothelial cells release a diffusible contractile factor distinct from endothelin. Gaine, S.P., Hales, M.A., Flavahan, N.A. Am. J. Physiol. (1998) [Pubmed]
  9. Endothelin receptor changes in hypoxia-induced pulmonary hypertension in the newborn piglet. Gosselin, R., Gutkowska, J., Baribeau, J., Perreault, T. Am. J. Physiol. (1997) [Pubmed]
  10. Developmental expression of endothelin receptors in postnatal swine mesenteric artery. Su, B.Y., Reber, K.M., Nankervis, C.A. Pediatr. Res. (2004) [Pubmed]
  11. Mechanisms of endothelin-1-induced pulmonary vasodilatation in neonatal pigs. Pinheiro, J.M., Malik, A.B. J. Physiol. (Lond.) (1993) [Pubmed]
  12. Endothelin ETB receptors couple to two distinct signaling pathways in porcine kidney epithelial LLC-PK1 cells. Ozaki, S., Ihara, M., Saeki, T., Fukami, T., Ishikawa, K., Yano, M. J. Pharmacol. Exp. Ther. (1994) [Pubmed]
  13. Paracrine endothelin signaling in the control of basal cell proliferation in guinea pig tracheal epithelium. Ninomiya, H., Inui, T., Masaki, T. J. Pharmacol. Exp. Ther. (1998) [Pubmed]
  14. Influence of regional differences in ETA and ETB receptor subtype proportions on endothelin-1-induced contractions in porcine isolated trachea and bronchus. Goldie, R.G., D'Aprile, A.C., Cvetkovski, R., Rigby, P.J., Henry, P.J. Br. J. Pharmacol. (1996) [Pubmed]
  15. Evidence for the presence of endothelin ETA receptors in endothelial cells in situ on the aortic side of porcine aortic valve. Nishimura, J., Aoki, H., Chen, X., Shikasho, T., Kobayashi, S., Kanaide, H. Br. J. Pharmacol. (1995) [Pubmed]
  16. Mechanisms of endothelin-induced venoconstriction in isolated guinea pig mesentery. Johnson, R.J., Fink, G.D., Galligan, J.J. J. Pharmacol. Exp. Ther. (1999) [Pubmed]
  17. Block of endothelin-1-induced release of thromboxane A2 from the guinea pig lung and nitric oxide from the rabbit kidney by a selective ETB receptor antagonist, BQ-788. D'Orléans-Juste, P., Claing, A., Télémaque, S., Maurice, M.C., Yano, M., Gratton, J.P. Br. J. Pharmacol. (1994) [Pubmed]
  18. Prevention of pulmonary vascular remodeling and of decreased BMPR-2 expression by losartan therapy in shunt-induced pulmonary hypertension. Rondelet, B., Kerbaul, F., Van Beneden, R., Hubloue, I., Huez, S., Fesler, P., Remmelink, M., Brimioulle, S., Salmon, I., Naeije, R. Am. J. Physiol. Heart Circ. Physiol. (2005) [Pubmed]
  19. Role and mechanism of endothelin-B receptors in mediating ET-1-induced vasoconstriction in pig skin. Pang, C.Y., Zhang, J., Xu, H., Lipa, J.E., Forrest, C.R., Neligan, P.C. Am. J. Physiol. (1998) [Pubmed]
  20. Effects of bosentan on neointimal response following coronary angioplasty. Sanmartín, M., Fernández-Ortiz, A., Fantidis, P., Aragoncillo, P., Fernández-Durango, R., Rollín, R., Alfonso, F., Hernández, R., Escaned, J., Macaya, C. Eur. J. Clin. Invest. (2003) [Pubmed]
  21. Hepatoprotective effect of a nonselective endothelin receptor antagonist (TAK-044) in the transplanted liver. Yamanaka, N., Takaya, Y., Oriyama, T., Furukawa, K., Tanaka, T., Tanaka, W., Ichikawa, N., Yasui, C., Ando, T., Yamanaka, J., Kuroda, N., Ko, M., Takada, M., Imakita, M., Kitayama, Y., Okamoto, E., Sasaki, S., Nakagaki, I., Hori, S., Ito, T. J. Surg. Res. (1997) [Pubmed]
WikiGenes - Universities