scholarly journals Activation of native TRPC1/C5/C6 channels by endothelin-1 is mediated by both PIP3and PIP2in rabbit coronary artery myocytes

2009 ◽  
Vol 587 (22) ◽  
pp. 5361-5375 ◽  
Author(s):  
Sohag N. Saleh ◽  
Anthony P. Albert ◽  
William A. Large
Keyword(s):  
Coronary Artery ◽  
Endothelin 1 ◽  
Rabbit Coronary Artery

Acute effect of 17 beta-estradiol on rabbit coronary artery contractile responses to endothelin-1

1992 ◽  
Vol 263 (1) ◽  
pp. H271-H275 ◽  
Author(s):  
C. Jiang ◽  
P. M. Sarrel ◽  
P. A. Poole-Wilson ◽  
P. Collins
Keyword(s):  
Coronary Artery ◽  
Coronary Arteries ◽  
Calcium Influx ◽  
Acute Effect ◽  
Bay K 8644 ◽  
Endothelin 1 ◽  
Independent Mechanism ◽  
Rabbit Coronary Artery ◽  
The Right ◽  
Dose Dependent

We assessed the acute effect of 17 beta-estradiol on coronary artery constrictor responses to endothelin-1. 17 beta-Estradiol significantly shifted endothelin-1, calcium, or BAY K 8644 concentration-dependent contraction curves to the right in endothelium-denuded coronary arteries isolated from nonpregnant female rabbits. The -log 50% effective dose (ED50) of calcium in high KCl medium (100 mM) was 3.8 +/- 0.11 in control and 3.2 +/- 0.1 and 2.8 +/- 0.12 after incubation with 17 beta-estradiol (1 and 10 microM, respectively). The -log ED50 of BAY K 8644 (KCl 15 mM) was 7.8 +/- 0.1 in control and 7.4 +/- 0.08 and 7.2 +/- 0.05 in the presence of 17 beta-estradiol (1 and 10 microM, respectively). The -log ED50 of endothelin-1 was 9.2 +/- 0.08 in control and 8.8 +/- 0.1, 8.4 +/- 0.07, and 8.1 +/- 0.12 after incubation with 17 beta-estradiol (3, 10, and 30 microM, respectively). Similar results were obtained from coronary arteries of male rabbits. These increases of -log ED50 values were significant (P less than 0.05 or 0.01). 17 beta-Estradiol and verapamil induced dose-dependent relaxation in both endothelium-intact or -denuded coronary arteries submaximally precontracted by endothelin-1. NG-monomethyl-L-arginine had no effect on relaxation induced by 17 beta-estradiol, whereas it eliminated relaxation induced by acetylcholine in rings with an intact endothelium. These data suggest that 17 beta-estradiol attenuates the rabbit coronary artery contraction induced by endothelin-1 via an endothelium-independent mechanism, possibly by affecting calcium influx.

scholarly journals Endothelin-1 activates a Ca2+-permeable cation channel with TRPC3 and TRPC7 properties in rabbit coronary artery myocytes

2007 ◽  
Vol 580 (3) ◽  
pp. 755-764 ◽  
Author(s):  
C. M. Peppiatt-Wildman ◽  
A. P. Albert ◽  
S. N. Saleh ◽  
W. A. Large
Keyword(s):  
Coronary Artery ◽  
Cation Channel ◽  
Endothelin 1 ◽  
Rabbit Coronary Artery

Dynamic Exercise Induces Elevation of Plasma Levels of Endothelin-1 in Patients with Coronary Artery Disease

Angiology ◽  
1995 ◽  
Vol 46 (9) ◽  
pp. 819-826 ◽  
Author(s):  
C. Letizia ◽  
F. Barillà ◽  
S. Cerci ◽  
C. D'Ambrosio ◽  
S. Coassin ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Plasma Levels ◽  
Dynamic Exercise ◽  
Endothelin 1 ◽  
Artery Disease

scholarly journals Genetic susceptibility of five tagSNPs in the endothelin-1 (EDN1) gene to coronary artery disease in a Chinese Han population

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Li-li Liang ◽  
Lin Chen ◽  
Meng-yuan Zhou ◽  
Meng-yun Cai ◽  
Jie Cheng ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chinese Han Population ◽  
Chinese Han ◽  
Han Population ◽  
Endothelin 1 ◽  
Increased Risk ◽  
Artery Disease ◽  
Cad Risk

Endothelin-1 (ET-1) plays important roles in endothelial dysfunction, vascular physiology, inflammation, and atherosclerosis. Nonetheless, the role of ET-1 (EDN1) gene variants on coronary artery disease (CAD) risk remains poorly understood. The aim of the present study was to evaluate the role of EDN1 gene polymorphisms on individual susceptibility to CAD. We genotyped five tagSNPs (single-nucleotide polymorphisms) (rs6458155, rs4145451, rs9369217, rs3087459, and rs2070699) within EDN1 gene in 525 CAD patients and 675 control subjects. In a multivariate logistic regression analysis, we detected an association of rs6458155 in EDN1 gene with the CAD risk; compared with the TT homozygotes, the CT heterozygotes (odds ratio (OR) = 1.53, 95% confidence interval (CI) = 1.02–2.29, P=0.040) and the CC homozygotes (OR = 1.55, 95% CI = 1.01–2.36, P=0.043) were statistically significantly associated with the increased risk for CAD. A similar trend of the association was found in dominant model (OR = 1.53, 95% CI = 1.05–2.25, P=0.029). Consistently, the haplotype rs6458155C-rs4145451C containing rs6458155 C allele exhibited the increased CAD risk (OR = 1.22, 95% CI = 1.03–1.43, and P=0.018). In addition, CT genotype of rs6458155 conferred the increased plasma ET-1 levels compared with TT genotype (P<0.05). No association of the other four tagSNPs in EDN1 gene with CAD risk was observed. In conclusion, our study provides the first evidence that EDN1 tagSNP rs6458155 is associated with CAD risk in the Chinese Han population, which is probably due to the influence of the circulating ET-1 levels.

Does coronary vasodilation after adenosine override endothelin-1-induced coronary vasoconstriction?

2007 ◽  
Vol 292 (1) ◽  
pp. H496-H502 ◽  
Author(s):  
Catalin Loghin ◽  
Stefano Sdringola ◽  
K. Lance Gould
Keyword(s):  
Animal Model ◽  
Coronary Artery ◽  
Myocardial Perfusion ◽  
Diagnostic Imaging ◽  
Perfusion Imaging ◽  
Myocardial Scar ◽  
Adenosine Stress ◽  
Stress Perfusion ◽  
Endothelin 1 ◽  
Perfusion Defects

Endothelin-1 is a powerful coronary vasoconstrictor that is overexpressed in coronary artery disease. Adenosine is a powerful coronary vasodilator used for myocardial perfusion imaging to identify flow-limiting coronary artery stenosis. Therefore, in an animal model we tested the hypothesis that intracoronary endothelin-1 may cause myocardial perfusion abnormalities by positron emission tomography (PET) at resting conditions that may persist or only partially improve after intravenous adenosine stress in the absence of myocardial scar and flow-limiting stenosis. Fourteen dogs underwent serial PET perfusion imaging with rubidium-82 before and after subselective intracoronary infusion of endothelin-1, followed by intravenous and then intracoronary adenosine. Small physiological doses of endothelin-1 infused into the mid-left circumflex coronary artery caused quantitatively significant resting perfusion abnormalities that normalized after intracoronary adenosine but not consistently after intravenous adenosine used for diagnostic imaging. After effects of adenosine abated, resting perfusion defects returned, lasting up to 5 h in some animals. Cumulative doses of endothelin-1 caused perfusion defects that did not normalize after intravenous adenosine. In an animal model without myocardial scar or flow-limiting stenosis, intracoronary endothelin-1 causes visually apparent, quantitatively significant, long-lasting myocardial perfusion defects at resting conditions that may persist or only partially improve after intravenous adenosine used for diagnostic imaging. These results may potentially explain resting perfusion abnormalities or heterogeneity by clinical PET that may persist or only partially improve after adenosine stress perfusion imaging in the absence of myocardial scar and flow-limiting stenosis.

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