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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 and John J. V. McMurray, BSc, MD, FRCP, FESC, FACC^*

^* Clinical Research Initiative in Heart Failure, University of Glasgow, Glasgow, Scotland UK
Medical Research Council Blood Pressure Group, Department of Medicine and Therapeutics, Western Infirmary, Glasgow, Scotland UK

View larger version (22K): [in a new window]   Figure 1 Response to AI (10–11M to 3 x 10–6M) in arteries from patients with CHF in the presence of vehicle, enalaprilat, chymostatin or both chymostatin and enalaprilat. AI = angiotensin I; CHF = chronic heart failure; KPSS = Kreb’s solution with KCl substituted for NaCl on an equimolar basis.

View larger version (20K): [in a new window]   Figure 2 Response to AI (10–11M to 3 x 10–6M) in arteries from patients with CHD in the presence of vehicle, enalaprilat, chymostatin or both chymostatin and enalaprilat. AI = angiotensin I; CHD = coronary heart disease. KPSS = Kreb’s solution with KCl substituted for NaCl on an equimolar basis.