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Marked bradykinin-induced tissue plasminogen activator release in patients with heart failure maintained on long-term angiotensin-converting enzyme inhibitor therapy

Fraser N. Witherow, MB, ChB, MRCP^*, Pamela Dawson, HNC, Christopher A. Ludlam, MB, ChB, PhD, FRCP, FRCPath, Keith A. A. Fox, BSc (Hons), MB, ChB, FRCP, FESC^* and David E. Newby, BA, BSc (Hons), PhD, BM, DM, MRCP^*,*

^* Cardiovascular Research, University of Edinburgh, Royal Infirmary of Edinburgh, Edinburgh, Scotland, United Kingdom
Department of Haematology, Royal Infirmary of Edinburgh, Edinburgh, Scotland, United Kingdom

View larger version (16K): [in a new window]   Figure 1 Effect of intra-arterial bradykinin and substance P infusions on blood flow and plasma tissue-type plasminogen activator (t-PA) antigen (solid lines) and activity (dashed lines) concentrations in the infused (solid symbols) and noninfused (open symbols) arms in the presence (left) or absence (right) of angiotensin-converting enzyme (ACE) inhibition. *p < 0.05 by analysis of variance (ANOVA). p < 0.001 by ANOVA for long-term ACE inhibition versus no ACE inhibition.

View larger version (13K): [in a new window]   Figure 2 Estimated net release of tissue-type plasminogen activator (t-PA) antigen (solid lines) and activity (dashed lines) during bradykinin (right) and substance P (left) infusions in the presence (solid circles) or absence (open circles) of angiotensin-converting enzyme (ACE) inhibition. p < 0.01 by analysis of variance (ANOVA) for all responses. *p < 0.001 by ANOVA for long-term ACE inhibition versus no ACE inhibition.