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Angiotensin Converting Enzyme (ACE) Journal of the American College of Cardiology Vol. 37, No. 4, 2001 © 2001 by the American College of Cardiology ISSN 0735-1097/01/$20.00 Published by Elsevier Science Inc. PII S0735-1097(01)01111-1 Angiotensin Converting Enzyme (ACE) and Non-ACE Dependent Angiotensin II Generation in Resistance Arteries From Patients With Heart Failure and Coronary Heart Disease Mark C. Petrie, BSC, MB, CHB, MRCP,* Neal Padmanabhan, MA, BM, BCH, MRCP,† John E. McDonald, BSC, MB, CHB, MRCP,*† Chris Hillier, BSC,PHD,* John M. C. Connell, MD, FRCP,† John J. V. McMurray, BSC, MD, FRCP, FESC, FACC* Glasgow, United Kingdom OBJECTIVES We sought to demonstrate non-angiotensin converting enzyme (ACE) dependent angioten- sin II (AII) generating pathways in resistance arteries from patients with chronic heart failure (CHF). BACKGROUND Non-ACE dependent AII generation occurs in resistance arteries from normal volunteers. Inhibition of non-ACE dependent AII generation may have therapeutic potential in CHF. METHODS Resistance arteries were dissected from gluteal biopsies from patients with coronary heart disease (CHD) and preserved left ventricular function and from patients with CHF. Using wire myography, concentration response curves to angiotensin I (AI) and AII were constructed in the presence of 1) vehicle, 2) chymostatin [an inhibitor of chymase], 3) enalaprilat, and 4) the combination of chymostatin and enalaprilat. RESULTS In resistance arteries from patients with CHD, the vasoconstrictor response to AI was not inhibited by either inhibitor alone (chymostatin [p Ն 0.05] or enalaprilat [p Ն 0.05]) but was significantly inhibited by the combination (p Ͻ 0.001). In arteries from patients with CHF, AI responses were inhibited by enalaprilat (p Ͻ 0.05) but not by chymostatin alone (p Ͼ 0.05). The combination of chymostatin and enalaprilat markedly inhibited the response to AI (p Ͻ 0.001) to a greater degree than enalaprilat alone (p Յ 0.01). CONCLUSIONS Non-ACE dependent AII generating pathways exist in resistance arteries from patients with both CHF and CHD. In resistance arteries from patients with CHD, inhibition of either the ACE or chymase pathway alone has no effect on AII generation, and both pathways must be blocked before the vasoconstrictor action of AI is inhibited. In CHF, blockade of ACE results in marked inhibition of responses to AI, but this is enhanced by coinhibition of chymase. These studies suggest that full suppression of the renin-angiotensin system cannot be achieved by ACE inhibition alone and provide a rationale for developing future therapeutic strategies. (J Am Coll Cardiol 2001;37:1056–61) © 2001 by the American College of Cardiology The traditional view that angiotensin II (AII) formation is has recently been demonstrated by Voors et al. (5) in large solely dependent on angiotensin converting enzyme (ACE) arteries and by our group in small resistance arteries from has recently been challenged. Non-ACE dependent conver- normal human volunteers (6). sion of angiotensin I (AI) to AII has been demonstrated in Demonstration of this dual pathway for AII generation homogenates of human myocardial tissue (1,2). In vitro, has important potential implications for the treatment of a non-ACE dependent conversion of AI to AII is brought number of cardiovascular diseases, especially chronic heart about by one or more serine proteases. The most important failure (CHF). Blockade of the renin-angiotensin- of these is thought to be chymase (3,4) as non-ACE aldosterone system (RAAS) improves symptoms and sur- mediated AII formation is substantially blocked by chymase vival in heart failure (7,8), and greater inhibition brings inhibitors such as chymostatin (2). That these non-ACE about greater benefit (9). The current approach to RAAS pathways are functionally important in human blood vessels interruption is ACE inhibition. However, the existence of a dual pathway means that that AII generation might persist in CHF, despite ACE inhibition, and raises the possibility From the *Clinical Research Initiative in Heart Failure, University of Glasgow, Glasgow, Scotland; and the †Medical Research Council Blood Pressure Group, that either the syndrome itself, or ACE inhibition, might Department of Medicine and Therapeutics, Western Infirmary, Glasgow, Scotland. also up-regulate the alternative pathway. It is known that Dr. Petrie was the recipient of a British Heart Foundation Junior Research Fellowship treatment of CHF with an ACE inhibitor does not result in (FS/97031:1997), and Dr. Padmanabhan was the recipient of a Wellcome Trust Junior Research Fellowship. Also supported by the Medical Research Council long-term suppression of AII plasma levels (10). Further- (Programme Grants held by J.J.V.M. and J.M.C.C.) and the Chief Scientist Office of more, in one study of patients with CHF, deterioration in the Scottish Executive (project grant held jointly by J.J.V.M., J.M.C.C, N.P. and left ventricular (LV) function occurred despite ACE inhi- M.C.P.). Manuscript received August 4, 1999; revised manuscript received November 8, bition, and this was associated with plasma concentrations 2000, accepted December 13, 2000. of AII that not only failed to show suppression but were JACC Vol. 37, No. 4, 2001 Petrie et al. 1057 March 15, 2001:1056–61 ACE and Non-ACE AII Generation in CHF four-channel wire myograph (J.P. Trading, Aarhus, Den- Abbreviations and Acronyms mark). ACE ϭ angiotensin converting enzyme Experimental protocol. BLOOD SAMPLING, BIOPSY PROCE- ϭ ACh acetylcholine DURE AND ARTERY PREPARATION. After 15 min supine ϭ AI angiotensin I rest, blood was drawn from a cannula in an antecubital vein AII ϭ angiotensin II BK ϭ bradykinin for estimation of blood chemistry and serum cholesterol. CHD ϭ coronary heart disease Subcutaneous gluteal biopsies were then obtained from each CHF ϭ chronic heart failure patient under local anesthesia (1% lidocaine) by the method KPSS ϭ Kreb’s solution with KCl substituted for NaCl previously described (12). Dissected tissue was placed im- on an equimolar basis mediately into cold 0.9% NaCl and then transferred to cold LV ϭ left ventricle, left ventricular LVEF ϭ left ventricular ejection fraction Kreb’s solution (composition in mM: NaCl 118.4, KCl 4.7, NE ϭ norepinephrine MgSO4.H2O 1.2, KH2PO4 1.2. Na HCO3 24.9, CaCl2 RAAS ϭ renin-angiotensin-aldosterone system 2.5, glucose 11.1, EDTA 0.023, which gives a pH of 7.4 when gassed with a 5% CO2/95% O2 mixture). Where possible, four resistance arteries approximately 2 mm in elevated compared with those found in age and gender- length were dissected free of fat. Dissected arteries were matched controls without CHF (11). stored in Kreb’s solution overnight at 4°C. Approximately ␮ The objective of this study was to determine whether or 24 h after the biopsy they were mounted on two 40 m not non-ACE dependent AI to AII conversion occurs in the diameter stainless steel wires in a four-channel myograph in resistance arteries of patients with CHF who receive long- which the wires are attached to a force transducer and term treatment with ACE inhibitors. We also studied micrometer, respectively. The temperature was raised to whether or not non-ACE dependent AII generation occurs 37°C, and a gas mixture (composition above) was bubbled in in resistance arteries from patients with coronary heart for the duration of the experiment. Dissection of resistance disease (CHD) and preserved ventricular function who have arteries from gluteal biopsies and myography protocols were not been treated with ACE inhibitors. performed by an operator who was blind to the patient type (i.e., CHF or CHD). METHODS Myography protocol: ACE and chymase inhibition. Af- ter a rest period of 30 min, each artery was stretched at Patients. All patients with renal failure (creatinine Ͼ200 1-min intervals to determine the passive exponential wall ␮mol/l) and diabetes mellitus were excluded. Written in- tension-internal circumference (L) relationship. From the formed consent was obtained from each patient, and all Laplace equation, where P ϭ T/r (P is the effective pressure, protocols were approved by the local committee on medical T is the wall tension and r is the internal radius), the ethics. equivalent circumference (L100) for a transmural pressure of Patients with CHF. Ambulatory patients with New York 100 mm Hg was calculated for each vessel by an iterative Heart Association class II/III CHF were studied. All were computer method. Each vessel was then set to the normal- Ͼ ϭ ϫ ␲ on long-term ( 3 months) ACE inhibitor and diuretic ized internal diameter, L1 0.9 L100/ , at which treatment. The etiology of CHF was CHD in all cases, and contraction is thought to be optimal (13). each patient had an echocardiographic LV ejection fraction After the above normalization procedure, the arteries (LVEF) Ͻ40% (Simpson’s biplane method). All patients were exposed twice to KPSS (Kreb’s solution with KCl had suffered a previous myocardial infarction. The patient’s substituted for NaCl on an equimolar basis) and once to NE usual medication (including ACE inhibitor therapy) was 10 ␮M. After a plateau contraction had been attained with taken on the study morning. These patients underwent NE, ACh 3 ␮M was added to the bath in order to stimulate gluteal biopsy and study of subcutaneous resistance arteries. endothelium-dependent vasodilation. Vessels that were un- Patients with CHD. Patients with chronic stable angina able to contract to either KPSS or NE, or that showed no attending outpatient clinics were studied. All patients had relaxation to ACh (and were, therefore, considered to have preserved LV systolic function, determined as an echocar- no functionally intact endothelium), were discarded. diographic LVEF Ն40% (Simpson’s biplane method), and Vessels were then incubated for a further 30 min in either none was treated with an ACE inhibitor.
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