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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:911.)
© 2004 American Heart Association, Inc.

Vascular Biology

Effects of Exogenous and Endogenous Natriuretic Peptides on Forearm Vascular Function in Chronic Heart Failure

Matthias Schmitt; Prasad Gunaruwan; Nicola Payne; Justin Taylor; Leong Lee; Andrew J.M. Broadley; Angus K. Nightingale; John R. Cockcroft; Allan D. Struthers; John V. Tyberg; Michael P. Frenneaux

From the Wales Heart Research Institute (M.S., P.G., J.T., L.L., A.J.M.B., A.K.N., J.R.C., M.P.F.), Cardiff, UK; the Medical Data Research Centre (N.P.), Providence Health System, Ore; the Department of Clinical Pharmacology (A.D.S.), Ninewells Hospital, Dundee, UK; and the Department of Medicine and Medical Physiology (J.V.T.), University of Calgary, Alberta, Canada.

Correspondence to Dr Matthias Schmitt, University of Wales, College of Medicine, Department of Cardiology, Wales Heart Research Institute, Heath Park, Cardiff, UK CF14 4XN. E-mail matthschmitt{at}doctors.org.uk

Objective— Natriuretic peptides (NPs) reduce central venous pressure in patients with chronic heart failure (cHF) despite attenuation of arterial, renal, and humoral effects. This suggests a preserved venodilator response. This study had 4 aims: to compare the venodilator effects of human NPs in patients with cHF; to assess the contribution of basal ANP and BNP levels to regulation of forearm vascular volume (FVV); to test the hypothesis that venous ANP responsiveness is preserved in cHF; and to assess the involvement of endothelial nitric oxide-synthase (eNOS) in NP-induced vascular effects.

Methods and Results— Venous and arterial forearm vascular responses to incremental intra-arterial doses of ANP, Urodilatin, BNP, CNP, or the ANP receptor antagonist A71915 were studied in 53 patients and 11 controls. ANP receptor antagonism reduced FVV by 4.4%±1.2% (P<0.05). The forearm blood flow (FBF) response to ANP was significantly blunted in patients versus controls (P<0.01), whereas FVV increased similarly in both groups (maximum 14.7% and 13.4%, both P<0.001). The eNOS blockade reduced ANP-induced FBF changes in controls but not in patients (P<0.05), whereas similar reductions in FVV changes were seen in groups (both P<0.001).

Conclusions— In cHF venous, but not arterial, ANP responsiveness is preserved. Arterial endothelial dysfunction may contribute to NP resistance.

Key Words: veins • capacitance • receptor antagonism • A71915

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