Effect of endothelin-1 and endothelin receptor blockade on the release of microparticles

2016 ◽  
Vol 46 (8) ◽  
pp. 707-713 ◽  
Author(s):  
Christian Jung ◽  
Michael Lichtenauer ◽  
Bernhard Wernly ◽  
Marcus Franz ◽  
Bjoern Goebel ◽  
...  
Keyword(s):  
Receptor Blockade ◽  
Endothelin Receptor ◽  
Endothelin 1

Exaggerated coronary reactivity to endothelin-1 in diabetes: reversal with bosentan

2002 ◽  
Vol 80 (10) ◽  
pp. 980-986 ◽  
Author(s):  
Subodh Verma ◽  
Emi Arikawa ◽  
Sammy Lee ◽  
Aaron S Dumont ◽  
Linfu Yao ◽  
...  
Keyword(s):  
Heart Function ◽  
Coronary Perfusion Pressure ◽  
Diabetic Rats ◽  
Diabetic Heart ◽  
Coronary Perfusion ◽  
Receptor Blockade ◽  
Endothelin Receptor ◽  
Endothelin 1 ◽  
Streptozotocin Induced Diabetes ◽  
And Control

We previously demonstrated that chronic endothelin receptor blockade (with bosentan) improved functional cardiac performance in streptozotocin-diabetic rats, suggesting a novel role of endothelin-1 (ET-1) in modulating diabetic heart dysfunction. To gain insight into the mechanism(s) underlying this effect, we examined the coronary vascular responses to ET-1 in hearts from diabetic and control rats treated with or without bosentan. Rats were divided into control, control-treated, diabetic, and diabetic-treated groups. The control-treated and diabetic-treated groups received bosentan (100 mg·kg–1·d–1) for 8 weeks. Following treatment, hearts were isolated and perfused, and coronary reactivity to ET-1 was assessed by measuring the changes in coronary perfusion pressure in response to ET-1 (50 and 100 pM). Additionally, maximal coronary blood flow (assessed with 10–5 M adenosine) was measured in isolated perfused hearts. The key observation is that coronary reactivity to ET-1 was significantly higher in the diabetic than the control rats. This effect was normalized in diabetic rats chronically receiving bosentan. Maximal coronary vasodilation did not differ between the four groups. In conclusion, the reactivity of ET-1 is altered in the isolated perfused coronary vascular bed from diabetic rats, and chronic ET receptor blockade restores this reactivity to control values. These observations provide a possible mechanism for the improvement in diabetic heart function observed after chronic bosentan treatment.Key words: endothelin-1, streptozotocin-induced diabetes, bosentan, endothelin receptor antagonist, coronary artery.

Augmented endothelial uptake of oxidized low-density lipoprotein in response to endothelin-1

2002 ◽  
Vol 103 (s2002) ◽  
pp. 9S-12S ◽  
Author(s):  
Henning MORAWIETZ ◽  
Nicole DUERRSCHMIDT ◽  
Bernd NIEMANN ◽  
Jan GALLE ◽  
Tatsuya SAWAMURA ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Receptor Blockade ◽  
Low Density ◽  
Pathophysiological Mechanism ◽  
Endothelin Receptor ◽  
Oxidized Low Density Lipoprotein ◽  
Endothelin 1 ◽  
Atherosclerotic Lesions

Endothelin-1 (ET-1) may be involved in the development and progression of atherosclerosis. Furthermore, endothelin receptor blockade was shown to reduce the formation of atherosclerotic lesions in experimental studies. Another potent pro-atherosclerotic risk factor is oxidized low-density lipoprotein (oxLDL). Endothelial cells mediate the uptake of oxLDL by the recently identified lectin-like oxLDL receptor-1 (LOX-1), which accumulates in atherosclerotic lesions. In the present study, we analysed the effects of ET-1 on oxLDL uptake and LOX-1 expression in primary cultures of human umbilical vein endothelial cells (HUVEC). ET-1 stimulated uptake of oxLDL in HUVEC, which reached a maximum after 1h. In further studies, we found a similar induction of LOX-1 mRNA and protein expression in response to ET-1. The augmented oxLDL uptake and the increased LOX-1 expression in response to ET-1 are mediated by the endothelin receptor B. Our data support a new pathophysiological mechanism by which locally and systemically increased ET-1 levels, e.g. in hypertensive patients, could promote LOX-1-mediated oxLDL uptake in human endothelial cells. This mechanism could promote the development and progression of endothelial dysfunction and atherosclerosis. In addition, endothelin receptor blockade could be considered as a new anti-atherosclerotic therapeutic principle.

RENAL ACTIONS OF ENDOTHELIN-1 UNDER ENDOTHELIN RECEPTOR BLOCKADE BY BE-18257B

1998 ◽  
Vol 159 (2) ◽  
pp. 563-566 ◽  
Author(s):  
Nabeel Syed ◽  
Frederick A. Gulmi ◽  
Shyan-Yih Chou ◽  
Unni M.M. Mooppan ◽  
Hong Kim
Keyword(s):  
Receptor Blockade ◽  
Endothelin Receptor ◽  
Endothelin 1

scholarly journals Gene Expression of Endothelin-1 and Endothelin Receptor A on Monocrotaline-Induced Pulmonary Hypertension in Rats After Bosentan Treatment

2010 ◽  
Vol 40 (9) ◽  
pp. 459 ◽  
Author(s):  
Kyoung Ah Lim ◽  
Kwan Chang Kim ◽  
Min-Sun Cho ◽  
Bo En Lee ◽  
Hae Soon Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pulmonary Hypertension ◽  
Endothelin Receptor ◽  
Endothelin 1 ◽  
Endothelin Receptor A
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