Different effects of angiotensin-converting enzyme inhibition in human arteries and veins

• Published in: Journal of cardiovascular pharmacology Vol. 22 Suppl 5; p. S17
• Main Authors: Yang, Z, Arnet, U, von Segesser, L, Siebenmann, R, Turina, M, Lüscher, T F
• Format: Journal Article
• Language: English
• Published: United States 1993
• Subjects: Acetylcholine - pharmacology; Angiotensin I - pharmacology; Angiotensin II - antagonists & inhibitors; Angiotensin-Converting Enzyme Inhibitors - pharmacology; Biphenyl Compounds - pharmacology; Bradykinin - pharmacology; Enalaprilat - pharmacology; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiology; Humans; Imidazoles - pharmacology; In Vitro Techniques; Losartan; Mammary Arteries - drug effects; Mammary Arteries - physiology; Muscle Contraction - drug effects; Muscle Relaxation - drug effects; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - physiology; Norepinephrine - pharmacology; Saphenous Vein - drug effects; Saphenous Vein - physiology; Tetrazoles - pharmacology
• ISSN: 0160-2446
• DOI: 10.1097/00005344-199322005-00004

The renin-angiotensin system (RAS) participates in the regulation of vascular tone; its effects were studied in human internal mammary artery (IMA) and saphenous vein (SV) suspended in organ chambers for isometric tension recording. The angiotensin-converting enzyme (ACE) inhibitor enalaprilat (10(-7) M) markedly augmented endothelium-dependent relaxations to bradykinin in SV (concentration shift: 10-fold; n = 6; p < 0.005), but not in IMA; in both blood vessels, it had no effect on endothelium-dependent relaxations to acetylcholine. The contractions to angiotensin I (Ang I; 10(-7) M) were markedly inhibited by enalaprilat (10(-7) M) in SV (control: 34 +/- 6% of 100 mM KCl; treatment: 18 +/- 6%; n = 7; p < 0.05) but not in IMA (control: 33 +/- 4%; treatment: 30 +/- 6%; n = 7; NS) and abolished by the Ang II receptor antagonist DuP 753 (10(-7) M) in both blood vessels. Ang II (10(-7) M) induced more pronounced contractions than Ang I in IMA (63 +/- 4%) and SV (63 +/- 5%; n = 5-6; p < 0.05 vs. Ang I), which was markedly inhibited by DuP 753 (10(-7) M; IMA: 21 +/- 5%; SV: 32 +/- 5%; p < 0.05). Thus, in SV but not IMA, ACE inactivates bradykinin and thereby blunts endothelium-dependent relaxations to the peptide and converts Ang I to Ang II.