Previous studies have demonstrated distal coronary vasoconstriction immediately after
percutaneous transluminal coronary angioplasty (PTCA). It was presumed that this coronary
vasoconstriction is the result of intimal injury or endothelial dysfunction,
1
abnormal autoregulatory tone,
2
,
3
,
4
formation of vasoactive substances,
5
,
6
impaired release of endothelial-derived relaxing factor,
7
and activation of adrenergic neural reflexes.
8
Endothelin-1 (ET-1) levels have been found to be elevated after PTCA.
9
ET-1 produces very potent and marked vasoconstriction in vitro as well as in vivo.
ET-1 binds to at least 2 receptors: in blood vessels, endothelin A (ETA) receptors are present only on vascular smooth muscle cells and cause contraction,
whereas endothelin B receptors are on endothelium, causing vasodilatation, and on
vascular smooth muscle cells, causing contraction. In healthy men, the major receptor
causing vasoconstriction, at least in the systemic circulation, is the ETA receptor.
11
,
12
,
13
Endogenously produced ET-1 contributes to the maintenance of basal coronary artery
tone in humans with and without coronary artery disease.
14
The aim of this study was to test the hypothesis that ETA receptor stimulation contributes to the coronary artery vasoconstriction observed
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Article info
Publication history
Accepted:
November 6,
2000
Received in revised form:
November 6,
2000
Received:
September 7,
2000
Identification
Copyright
© 2001 Excerpta Medica Inc. Published by Elsevier Inc. All rights reserved.