1. ¹Institute of Clinical Chemistry and Pathobiochemistry, Justus Liebig University, Giessen, Germany
2. ²Clinic for Cardiovascular Surgery, Justus Liebig University, Giessen, Germany
3. ³Institute of Pathological Biochemistry, Otto-von-Guericke-University, Magdeburg, Germany

Correspondence: Dr N Al-Fakhri, Institute of Clinical Chemistry and Pathobiochemistry, Justus Liebig University, Gaffkystrae 11, 35392 Giessen, Germany. E-mail: nadia.al-fakhri@klinchemie.med.uni-giessen.de

⁴Current address Medical Center for Ecology, Justus Liebig University, Giessen, Germany.

Received 28 June 2002; Revised 24 October 2001; Accepted 2 November 2002.

Abstract

The objective was to investigate whether the renin–angiotensin (RA) system and related peptides endothelin-1 (ET-1) and vasopressin (VP) influence the development of coronary artery disease (CAD). Angiotensin I-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism has been associated with the risk of CAD. The ACE I/D polymorphism determines ACE activity, but plasma levels of other RA system components remain unchanged. However, ET-1 and VP production could be increased by RA system-dependent stimulation, continually promoted by paracrine stimulation and sustained by neointimal growth. ET-1 and VP have not been associated with the ACE I/D polymorphism so far. The present study investigated the association of the ACE I/D polymorphism with plasma concentrations of ET-1 and VP, as well as with renin, angiotensin-II (AT-II) and ACE activity in 98 Caucasian individuals with CAD. ACE I/D polymorphism showed no association with plasma levels of VP, ET-1, AT-II or renin. These parameters were also not associated taking into consideration different patient variables, such as diabetes mellitus, hypertension or severity of CAD. Only plasma ACE activity was associated with the D allele. In conclusion, the ACE I/D polymorphism could not be related to plasma concentrations of VP, ET-1, renin or AT-II, but as previously demonstrated, it could only be related to ACE activity in patients with CAD. Differences in ACE activity between ACE I/D genotype subgroups are probably compensated within the RA system itself or within non-ACE pathways, so that plasma concentrations of the related peptides ET-1 and VP remain unaffected.