Coronary vasoconstriction after coronary angioplasty is attenuated by endothelin a receptor antagonism

Kyriakides, Zenon S.; Kremastinos, Dimitrios Th.; Psychari, Stavroula N.; Kolettis, Theofilos M.; Sbarouni, Eftihia; Webb, David J.

doi:10.1016/s0002-9149(01)01441-2

Cited by 18 publications

(11 citation statements)

References 20 publications

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“…Acute administration of ET-1 receptor antagonists showed favourable effects on coronary vasodilating properties in patient with coronary artery disease [187,188]. Improved endothelial function has been reported after ET-1 receptor blockade in atherosclerotic patients treated with ACE-inhibitors, suggesting an additive beneficial effects on endothelial function [189].…”

Section: Endothelin Receptors Antagonistsmentioning

confidence: 99%

Restoring the Dysfunctional Endothelium

Osto¹,

Coppolino²,

Volpe³

et al. 2007

CPD

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Nowadays the endothelium is considered a key determinant of vascular health. NO is the principal mediator of all endothelial protective effects, due to its antiinflammatory, antiproliferative, immunomodulatory and vasorelaxant properties. On the contrary, a growing body of evidence suggests that endothelial dysfunction is associated with cardiovascular events. Emerging data suggest that acute coronary syndromes (ACS) may involve a complex interplay between endothelial dysfunction, inflammation and thrombosis. Despite the success in reducing the mortality from acute cardiovascular events, the incidence of cardiovascular disease and its complication continues to increase. New insights into mechanisms of endothelial dysfunction, such as a better understanding of the regulation of vascular sources of oxygen radicals, may lead to novel therapeutic strategies with the potential to improve prognosis. The key pharmacological agents that improve clinical outcome in high-risk patients are statins, ACE-inhibitors or angiotensin receptor antagonists. Compelling scientific evidence suggests that these medications are effective in improving endothelial function. The present review focuses on the potential importance of benefits on endothelium of these medicaments in the management of acute coronary syndromes.

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Section: Endothelin Receptors Antagonistsmentioning

confidence: 99%

Restoring the Dysfunctional Endothelium

Osto¹,

Coppolino²,

Volpe³

et al. 2007

CPD

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“…60 The selective ET A receptor blocker BQ-123 given to patients with stable angina was shown to prevent distal coronary vasoconstriction after percutaneous transluminal coronary angioplasty. 61 …”

Section: Coronary Artery Diseasementioning

confidence: 99%

Endothelin Receptor Blockers in Cardiovascular Disease

Rich¹,

McLaughlin²

2003

Circulation

199

126

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Abstract-The endothelin (ET) system is comprised of 4 active ETs, with ET-1 being the predominant isoform in the cardiovascular system. Because of the potent vasoconstricting and mitogenic effects of ET-1 and its involvement in various cardiovascular diseases, blockade of the ET receptor has received considerable attention. ET receptor antagonism has been demonstrated to be beneficial in patients with pulmonary hypertension. The nonselective ET receptor antagonist bosentan improves exercise capacity and increases time to clinical worsening in patients with pulmonary arterial hypertension. Key Words: endothelin Ⅲ heart failure Ⅲ pulmonary heart disease T he endothelin (ET) system, like other vascular regulatory systems, consists of a parent peptide that undergoes enzymatic activation and exerts its biologic effects by modulating specific receptors. Of the 4 active ETs (ET 1 through 4), ET-1 is the predominant isoform in the cardiovascular system, which is generated through the cleavage of prepro ET-1 to big ET-1 and then to ET-1 by the action of ET-converting enzymes. ET-1 is found in endothelial cells and is released toward the vascular smooth muscle consistent with a paracrine role, but it is also produced by smooth muscle cells and cardiomyocytes. 1,2 ET-1 has vasoconstrictive and mitogenic effects, stimulates the production of growth factors such as vascular endothelial growth factor and basic fibroblast growth factor, and potentiates the effects of transforming growth factor-␤ and platelet-derived growth factor. 3-7 Chronic ET-1 stimulation can result in myocardial fibrosis and hypertrophy and vascular fibrosis with extracellular matrix proliferation. 8 In the lung, ET-1 is abundantly expressed in the pulmonary vasculature and appears to play an important role in the regulation of pulmonary vascular tone. 9 ET-1 is also produced in leukocytes where it influences the production of a wide range of cytokines in the inflammatory response. 10 ET is regulated in an autocrine fashion by physiochemical factors such as blood flow, pulsatile stretch, sheer stress, and pH. 11-13 Acute hypoxia leads to selective stimulation of the ET-1 gene and ET synthesis in the pulmonary vasculature. 14 ET-1 biosynthesis is also stimulated by low-density lipoprotein cholesterol and glucose, and thrombin. 15,16 Endogenous inhibitors of ET-1 synthesis include nitric oxide, prostacyclin, atrial natriuretic peptides, and estrogens. [17][18][19][20] ET-1 exerts its major vascular effects through activation of 2 distinct G protein coupled ET A and ET B receptors. ET A receptors are found in the medial smooth muscle layers of the blood vessels, and atrial and ventricular myocardium. 21 When stimulated, the ET A receptors induce vasoconstriction and cellular proliferation by increasing intracellular calcium.ET B receptors are localized on endothelial cells and, to some extent, smooth muscle cells and macrophages. 22 The activation of ET B receptors stimulates the release of nitric oxide and prostacyclin and prevents apoptosis. 23 Normally, t...

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“…Coronary vasoconstriction after coronary angioplasty has been attributed to a variety of mechanisms and it can be prevented by ET A receptor blockade. Quantitative analysis of coronary angiography of the diameter of the distal segment of coronary arteries 25 minutes after coronary angioplasty, showed that intracoronary administration of BQ-123 hindered vasoconstriction of the distal segment [16] (Figure 5).…”

Section: Et-1 During Angioplastymentioning

confidence: 99%

Endothelin A-receptors and the coronary circulation

Polymeropoulos¹,

Valenti²,

Kyriakides³

2013

WJCD

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We review the role of endothelin (ET) A-receptors (R) on the coronary circulation. ET-1 maintains the normal coronary artery tone. ET-1 plasma levels are increased during and after coronary angioplasty and this increase is related to myocardial ischaemia rather than to mechanical artery injury. ET_AR antagonists inhibit coronary artery vasoconstriction induced by ET release after coronary angioplasty in humans. ET promotes neointimal formation and ET_AR antagonism has been shown to inhibit restenosis after angioplasty in the animal model but not in humans. ET_AR blockade increases coronary blood flow, dilates distal coronary arterial segments and decreases coronary vascular resistance. Coronary collaterals are less sensitive than other coronary vessels to ET-1. ET_AR blockade decreases collateral blood flow and, consequently, perfusion of the ischemic myocardium.

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Coronary vasoconstriction after coronary angioplasty is attenuated by endothelin a receptor antagonism

Cited by 18 publications

References 20 publications

Restoring the Dysfunctional Endothelium

Restoring the Dysfunctional Endothelium

Endothelin Receptor Blockers in Cardiovascular Disease

Endothelin A-receptors and the coronary circulation

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