Cited by 13Nitric Oxide and Endothelin EffectsRenin-Angiotensin System StudiesCardiovascular Health and Disease Prevention

Acute effects of ACE inhibition on coronary endothelial dysfunction

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Nickenig, Georg, Stäblein, Alexander, Wassmann, Sven, Wyen, Christoph, Müller, Cornelius, Böhm, Michael·2000·Journal of the Renin-Angiotensin-Aldosterone System

Abstract

The prerequisite of atherosclerosis, endothelial dysfunction, is characterised by impaired endothelium-dependent vasodilation caused by the reduced bioavailibility of nitric oxide (NO). In order to assess the role of acute ACE inhibition in this setting, coronary arterial endothelial function was quantified following acute intracoronary administration of the angiotensin-converting enzyme (ACE) inhibitor quinapril. Twenty-one patients with non-limiting coronary artery disease were studied before and after acute intracoronary administration of 10 mg quinapril. Nine patients received pre-treatment with the angiotensin AT 1 -receptor antagonist losartan (2x50 mg, p.o.). Coronary cross-sectional diameter was measured via quantitative angiography and microvascular reaction was investigated by intracoronary Doppler flow measurement during intracoronary infusion of 0.1 to 10 µmol/l acetylcholine. Quinapril acutely improved endothelial dysfunction on the macro- as well as the microvascular level. Losartan did not alter macrovascular function but facilitated microvascular endothelial function. Acute quinapril application led to no further improvement of endothelial dysfunction in patients pre-treated with losartan. Acute quinapril infusion improved endothelial function in patients with coronary heart disease. Treatment with the AT 1 -receptor antagonist losartan led to a slight improvement in microvascular endothelial function, but pre-treatment with losartan blunted the vascular effect of quinapril, suggesting that the combination of ACE inhibition and AT 1 -receptor antagonism may not exert a synergistic benefical impact on the coronary vasculature.

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Crossref · 10.3317/jraas.2000.067

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Authors
Nickenig, G., Stäblein, A., Wassmann, S., Wyen, C., Müller, C., & Böhm, M.
Affiliations
Universitätsklinikum des Saarlandes (DE)
Venue
Journal of the Renin-Angiotensin-Aldosterone System
Published
2000-12
Volume
1
Issue
4
Pages
361-364
ISSN
  • 1470-3203 (ISSN-L)
  • 1752-8976
OpenAlex
W2103018838
Cited by
13
References
21
Citations by year
2022: 1 · 2020: 1 · 2016: 1
FWCI
0.20
Type
journal article
Language
en
Open access
Locations
  • Journal of the Renin-Angiotensin-Aldosterone System (publishedVersion)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
Keywords
angiotensin-converting enzyme inhibition, quinapril, endothelial dysfunction, coronary endothelium, coronary microvascular function, acetylcholine-induced vasodilation, losartan, AT1 receptor antagonism, coronary artery disease, nitric oxide bioavailability, intracoronary infusion, combination therapy
MeSH terms
Quinapril, Angiotensin-Converting Enzyme Inhibitors, Coronary Circulation, Endothelium, Vascular, Female, Humans, Isoquinolines, Male, Microcirculation, Middle Aged, Time Factors, Vasodilation, Vasomotor System, Losartan, Tetrahydroisoquinolines, Receptor, Angiotensin, Type 1, Angiotensin Receptor Antagonists

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