title: Impaired endothelium-dependent and -independent vasodilation in elderly patients with chronic heart failure.
abstract: BACKGROUND
  Impaired endothelium-dependent and independent vasodilator responses in chronic heart failure (CHF) have been well described. Previous studies involved younger patients and omitted medications prior to study.
  
  
  OBJECTIVE
  We explored if new therapeutic interventions would restore vasodilator responses in typical patients with chronic heart failure.
  
  
  RESULTS
  24 patients and 15 controls were recruited, patients were maintained on their usual medications. Forearm blood flow responses were measured by venous occlusion plethysmography in response to incremental doses of sodium nitroprusside (SNP) (6, 9 and 12 nmol/min), acetylcholine (ACH) (120, 180 and 240 nmol/min), angiotensin II (AII) (1, 10 and 100 nmol/min) and N(g)-Nitro-L-arginine methyl ester (L-NAME) (1, 2 and 4 nmol/min) infused into the non-dominant brachial artery. FBF responses to SNP were impaired in patients compared with controls (13.7(9.9,17.4) vs. 24.8(18.6,30.9)) arbitrary units, P<0.001). Similarly FBF responses to ACH were reduced in patients compared with controls (7.5(4.2,10.9) vs. 24.8(16.4,33.2)) arbitrary units, P<0.001. Decreased FBF was noted in response to AII and L-NAME but was significant only for AII and did not differ between groups.
  
  
  CONCLUSIONS
  In elderly patients with CHF, endothelium-dependent and independent vasodilator responses were blunted compared with controls. Defects in nitric oxide bioavailability and smooth muscle responsiveness are not reversed by modern medical management of the heart failure syndrome.
authors.affiliation: Department of Therapeutics and Pharmacology, Whitla Medical Building, Queen's University, 97 Lisburn Road, Belfast BT9 7BL, UK.
authors.forename: David R
authors.initials: DR
authors.lastname: Morgan
authors.forename: Lana J
authors.initials: LJ
authors.lastname: Dixon
authors.forename: Colm G
authors.initials: CG
authors.lastname: Hanratty
authors.forename: Sinead M T
authors.initials: SM
authors.lastname: Hughes
authors.forename: William J
authors.initials: WJ
authors.lastname: Leahey
authors.forename: Keith P
authors.initials: KP
authors.lastname: Rooney
authors.forename: G Dennis
authors.initials: GD
authors.lastname: Johnston
authors.forename: Gary E
authors.initials: GE
authors.lastname: McVeigh
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage / Q000494:pharmacology; D000368:Aged; D000369:Aged, 80 and over; D019540:Area Under Curve; D016022:Case-Control Studies; D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D004791:Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D005260:Female; D005542:Forearm / Q000098:blood supply*; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000008:administration & dosage / Q000494:pharmacology; D009599:Nitroprusside / Q000008:administration & dosage / Q000494:pharmacology; D010991:Plethysmography; D012039:Regional Blood Flow / Q000187:drug effects; D013318:Stroke Volume / Q000187:drug effects; D006113:United Kingdom; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D004791:Enzyme Inhibitors; D014665:Vasodilator Agents; D009599:Nitroprusside; D000109:Acetylcholine; D019331:NG-Nitroarginine Methyl Ester