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Kiowski, W., Luscher, T.F., Linder, L. and Buhler, F.R. (1991) Endothelin-1-induced vasoconstriction in humans. Reversal by calcium channel blockade but not by nitrovasodilators or endothelium-derived relaxing factor. Circulation, 83, 469-475. doi:10.1161/01.CIR.83.2.469

has been cited by the following article:

• TITLE: Endothelin A-receptors and the coronary circulation

  AUTHORS: Evangelos Polymeropoulos, Mesele Valenti, Zenon S. Kyriakides

  KEYWORDS: Endothelin; Coronary Circulation

  JOURNAL NAME: World Journal of Cardiovascular Diseases, Vol.3 No.5, July 25, 2013

  ABSTRACT: 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. ETAR antagonists inhibit coronary artery vasoconstriction induced by ET release after coronary angioplasty in humans. ET promotes neointimal formation and ETAR antagonism has been shown to inhibit restenosis after angioplasty in the animal model but not in humans. ETAR 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. ETAR blockade decreases collateral blood flow and, consequently, perfusion of the ischemic myocardium.