title: Endothelial control of arterial distensibility is impaired in chronic heart failure.
abstract: BACKGROUND
  Vascular tone is a determinant of conduit artery distensibility. The aim of this study was to establish whether endothelium-derived relaxing factor (EDRF) influences the distensibility of conduit arteries and whether endothelium-mediated increases in distensibility are impaired in chronic heart failure (CHF).
  
  
  RESULTS
  Conduit artery distensibility was measured by two methods in healthy subjects and in nine patients with CHF caused by dilated cardiomyopathy. In the first method, pulse-wave velocity (PWV) was measured in the right common iliac artery at rest and during local infusions of acetylcholine (10(-7) to 10(-5) mol/L) or adenosine (2 x 10(-7) to 2 x 10(-5) mol/L), with correction for systemic effects. Acetylcholine induced concentration-dependent local reductions of PWV in healthy subjects (-5%, -15%, and -26%) but not in CHF patients (3%, 1%, -4%, P < .01), whereas adenosine induced similar reductions of PWV in healthy subjects and CHF patients. In the second method, brachial artery diameter, blood flow, and blood pressure were measured noninvasively by high-resolution ultrasound, continuous-wave Doppler, and photoplethysmography during reactive hyperemia in the hand and after sublingual glyceryl trinitrate (GTN, 400 micrograms). Hyperemic flow, similar in healthy subjects and CHF patients, was associated with increases in diameter and distensibility in healthy subjects (8.8% and 18.4%, respectively) but not in CHF patients (0.3% and -4.5%), whereas GTN induced similar effects in healthy subjects and CHF patients.
  
  
  CONCLUSIONS
  These data indicate that conduit artery distensibility is increased by acetylcholine and increased blood flow in healthy subjects but not in CHF patients, whereas the effects of adenosine and GTN on distensibility are preserved in CHF patients. This implies that EDRF-mediated increases in distensibility are impaired in CHF patients, thus adding to cardiac work.
authors.affiliation: Department of Cardiology, University of Wales College of Medicine, Heath Park, Cardiff, UK.
authors.forename: M W
authors.initials: MW
authors.lastname: Ramsey
authors.forename: J
authors.initials: J
authors.lastname: Goodfellow
authors.forename: C J
authors.initials: CJ
authors.lastname: Jones
authors.forename: L A
authors.initials: LA
authors.lastname: Luddington
authors.forename: M J
authors.initials: MJ
authors.lastname: Lewis
authors.forename: A H
authors.initials: AH
authors.lastname: Henderson
mesh_terms: D000109:Acetylcholine; D000241:Adenosine; D001783:Blood Flow Velocity / Q000187:drug effects; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000187:drug effects / Q000502:physiology; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology*; D016022:Case-Control Studies; D005260:Female; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D007083:Iliac Artery / Q000187:drug effects / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000502:physiology*; D005996:Nitroglycerin; D014463:Ultrasonography; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*; D014665:Vasodilator Agents
chemical_list: D014665:Vasodilator Agents; D009569:Nitric Oxide; D005996:Nitroglycerin; D000241:Adenosine; D000109:Acetylcholine