scholarly journals Enhanced endothelin receptor type B-mediated vasodilation and underlying [Ca2+]iin mesenteric microvessels of pregnant rats

2013 ◽  
Vol 169 (6) ◽  
pp. 1335-1351 ◽  
Author(s):  
Marc Q Mazzuca ◽  
Yiping Dang ◽  
Raouf A Khalil
Keyword(s):  
Receptor Type ◽  
Endothelin Receptor ◽  
Type B ◽  
Pregnant Rats ◽  
Mesenteric Microvessels

Abstract 052: Placental Growth Factor (PlGF) Reduces Blood Pressure and Improves Endothelin Type B Receptor (ETBR)-Mediated Microvascular Dilation in Hypertensive Pregnant Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Marc Q Mazzuca ◽  
Zongli Ren ◽  
Chen Lin ◽  
Jose S Possomato-Vieira ◽  
Minglin Zhu ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Mesenteric Arteries ◽  
Hypertensive Disorder ◽  
Type B ◽  
Pregnant Rats ◽  
Western Blots ◽  
New Approach ◽  
Nitrite Production ◽  
Uterine Perfusion ◽  
Mesenteric Microvessels

Preeclampsia is a pregnancy-related hypertensive disorder (HTN-Preg) with an imbalance between anti-angiogenic soluble fms-like tyrosine kinase-1 (sFlt-1) and angiogenic PlGF, but the vascular targets involved are unclear. We have shown downregulation of endothelial ET B R in Preg rats with reduced uterine perfusion pressure (RUPP), and studies have shown increased plasma sFlt-1 in RUPP rats. We tested if raising PIGF/sFlt-1 ratio by infusing PIGF (10 μg/kg/day) in RUPP rats would improve BP and microvascular ET B R signaling, and vice versa, if lowering PIGF/sFlt-1 ratio by infusing sFlt-1 (10 μg/kg/day) in Preg rats increases BP and reduces ET B R signaling. On day 19, BP was recorded and mesenteric microvessels were isolated for measurement of diameter and [Ca 2+ ] i (fura-2 340/380 ratio). BP was in PlGF-RUPP 105±2 < RUPP 126±1 and in sFlt-Preg 125±4 > Norm-Preg 97±5 mmHg. ET-1 vasoconstriction was in PlGF-RUPP 62.6±3.0 < RUPP 83.4±5.3 and in sFlt-Preg 76.1±4.7 > Norm-Preg 52.1±3.2%. ET-1 caused parallel increases in microvascular [Ca 2+ ] i that was in PlGF-RUPP 0.87±0.02 < RUPP 0.92±0.01 and in sFlt-Preg 0.93±0.02 > Norm-Preg 0.85±0.01. Endothelium removal or microvessel treatment with ET B R antagonist BQ-788 enhanced ET-1 vasoconstriction and [Ca 2+ ] i in Norm-Preg and PlGF-RUPP, but not RUPP or sFlt-Preg. The ET B R agonists sarafotoxin 6c (S6c) and IRL-1620 caused relaxation that was in PlGF-RUPP 42.9±10.8, 38.0±11.2% > RUPP 4.7±3.4, 7.5±2.3% and in sFlt-Preg 3.1±1.0, 5.4±1.6% < Norm-Preg 29.9±7.8, 28.0±9.1%. L-NAME partially reduced ACh- and ET B R-induced relaxation in Norm-Preg, PlGF-RUPP, but not RUPP or sFlt-Preg, suggesting that PlGF improves the decreased NO-dependent and ET B R-mediated vasorelaxation in HTN-Preg. Basal, ACh-, S6c-, and IRL-1620-induced nitrate/nitrite production was enhanced in mesenteric arteries of PIGF-RUPP and Norm-Preg vs. RUPP rats. Western blots and immunohistochemistry revealed greater levels of endothelial ET B R in PlGF-RUPP and Norm-Preg vs. RUPP and sFlt-Preg. Thus improving PlGF/sFlt-1 balance reduces BP and ET-1 vasoconstriction, and enhances ET B R-mediated NO-dependent vasodilation in RUPP rats, and could be a new approach in the management of HTN-Preg.

scholarly journals Null mutation of the endothelin receptor type B gene causes embryonic death in the GK rat

PLoS ONE ◽  
2019 ◽  
Vol 14 (6) ◽  
pp. e0217132 ◽  
Author(s):  
Jinxi Wang ◽  
Ruihua Dang ◽  
Yoshiki Miyasaka ◽  
Kousuke Hattori ◽  
Daisuke Torigoe ◽  
...  
Keyword(s):  
Receptor Type ◽  
Null Mutation ◽  
Endothelin Receptor ◽  
Type B ◽  
Gk Rat ◽  
Embryonic Death

Renal endothelin receptor type B upregulation in rats with low or high renin hypertension

2004 ◽  
Vol 22 (9) ◽  
pp. 1797-1803
Author(s):  
Noureddine Brakch ◽  
Saad Abdel-Sayed ◽  
Flore Allemandou ◽  
Qing Wang ◽  
Jean F Aubert ◽  
...  
Keyword(s):  
Receptor Type ◽  
Endothelin Receptor ◽  
Type B

Physical mapping of the endothelin receptor type B to bovine chromosome 12

1997 ◽  
Vol 8 (5) ◽  
pp. 380-381 ◽  
Author(s):  
Jörg Schläpfer ◽  
Daniel S. Gallagher ◽  
Jay D. Burzlaff ◽  
Scott K. Davis ◽  
Jeremy F. Taylor ◽  
...  
Keyword(s):  
Physical Mapping ◽  
Bovine Chromosome ◽  
Receptor Type ◽  
Chromosome 12 ◽  
Endothelin Receptor ◽  
Type B

scholarly journals Differential expression of endothelin receptor type B in cancers of the breast.

2021 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Breast Cancer ◽  
Differential Expression ◽  
Survival Data ◽  
Normal Breast ◽  
Differentially Expressed ◽  
Receptor Type ◽  
Endothelin Receptor ◽  
Type B ◽  
Significant Differential Expression ◽  
Primary Tumors

Breast cancer affects women at relatively high frequency (1). We mined published microarray datasets (2, 3) to determine in an unbiased fashion and at the systems level genes most differentially expressed in the primary tumors of patients with breast cancer. We report here significant differential expression of the gene encoding endothelin receptor type B, EDNRB, when comparing primary tumors of the breast to the tissue of origin, the normal breast. EDNRB was also differentially expressed in the tumor cells of patients with triple negative breast cancer. EDNRB mRNA was present at significantly lower quantities in tumors of the breast as compared to normal breast tissue. Analysis of human survival data revealed that expression of EDNRB in primary tumors of the breast was correlated with overall survival in patients with luminal A subtype cancer, demonstrating a relationship between primary tumor expression of a differentially expressed gene and patient survival outcomes influenced by molecular subtype. EDNRB may be of relevance to initiation, maintenance or progression of cancers of the female breast.

scholarly journals Enteric nervous system development: migration, differentiation, and disease

2013 ◽  
Vol 305 (1) ◽  
pp. G1-G24 ◽  
Author(s):  
Jonathan I. Lake ◽  
Robert O. Heuckeroth
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Enteric Nervous System ◽  
System Development ◽  
Hirschsprung Disease ◽  
Nervous System Development ◽  
Receptor Type ◽  
Model Organisms ◽  
Endothelin Receptor ◽  
Type B

The enteric nervous system (ENS) provides the intrinsic innervation of the bowel and is the most neurochemically diverse branch of the peripheral nervous system, consisting of two layers of ganglia and fibers encircling the gastrointestinal tract. The ENS is vital for life and is capable of autonomous regulation of motility and secretion. Developmental studies in model organisms and genetic studies of the most common congenital disease of the ENS, Hirschsprung disease, have provided a detailed understanding of ENS development. The ENS originates in the neural crest, mostly from the vagal levels of the neuraxis, which invades, proliferates, and migrates within the intestinal wall until the entire bowel is colonized with enteric neural crest-derived cells (ENCDCs). After initial migration, the ENS develops further by responding to guidance factors and morphogens that pattern the bowel concentrically, differentiating into glia and neuronal subtypes and wiring together to form a functional nervous system. Molecules controlling this process, including glial cell line-derived neurotrophic factor and its receptor RET, endothelin (ET)-3 and its receptor endothelin receptor type B, and transcription factors such as SOX10 and PHOX2B, are required for ENS development in humans. Important areas of active investigation include mechanisms that guide ENCDC migration, the role and signals downstream of endothelin receptor type B, and control of differentiation, neurochemical coding, and axonal targeting. Recent work also focuses on disease treatment by exploring the natural role of ENS stem cells and investigating potential therapeutic uses. Disease prevention may also be possible by modifying the fetal microenvironment to reduce the penetrance of Hirschsprung disease-causing mutations.

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