© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Interactions among ACE, kinins and NO
aHoechst Marion Roussel, DG Cardiovascular, D-65926 Frankfurt/Main, Germany
bDepartment of Chemistry, Center for Biomedical Research, Oakland University, Rochester, MI 48309-4401, USA
* Corresponding author. Tel.: +49-69-305-6868, fax: +49-69-305-81252 wolfgang.linz@hmrag.com
Received 27 November 1998; accepted 2 February 1999
KEYWORDS ACE; kinins; NO; superoxide
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1 Introduction |
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Angiotensin converting enzyme (ACE) is a transmembrane zinc metallopeptidase that cleaves carboxy-terminal dipeptides from several peptides and is expressed in great amounts in vascular endothelial cells [1,2]. A soluble form of the enzyme is found in plasma which is presumably derived from the membrane-bound form by proteolytic cleavage [3]. ACE plays a major role in the regulation of the vascular tone by converting the biological inactive decapeptide angiotensin I (ANG I) into the vasoconstrictor and proliferative octapeptide angiotensin II (ANG II). In a similar manner, ACE inactivates the vasodilatory nonapeptide bradykinin (BK), which derives from a number of different sources [4].
Endothelium-derived or exogenously added BK exerts its vasodilatory action through stimulation of endothelial B2 kinin receptors thereby causing the synthesis and release of vasodilator substances such as endothelium-derived hyperpolarizing factor (EDHF) [5], prostacyclin and nitric oxide (NO) [6]. Many of the effects of NO
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2 Molecular and biochemical pathways |
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2.1 Modulation of ACE by NO
2.2 Effect of ACE inhibition on eNOS and NO
2.3 Effects of ACE inhibitors on B2 kinin receptors
2.4 Effects of angiotensin 1–7 on ACE and B2 kinin receptors
2.5 ANG II and the kinin/NO system
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3 Pathophysiological relevance |
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3.1 Hypertension
3.2 Atherosclerosis
3.3 Myocardial ischaemia
3.4 Myocardial infarction-remodeling
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4 Conclusion |
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