title: Renal vasodilatory effect of endothelial stimulation in patients with chronic congestive heart failure.
abstract: OBJECTIVE
  This study sought to examine the vasodilatory response of the renal circulation to endothelial stimulation in patients with chronic heart failure.
  
  
  BACKGROUND
  Renal blood flow is often reduced in patients with chronic congestive heart failure and may lead to deterioration of renal function. Stimulation of renal endothelium has been shown to cause renal vasodilation in animals and in isolated human renal artery. The vasoregulatory role of the renal endothelium in patients with heart failure has not been evaluated.
  
  
  METHODS
  Renal vasodilatory effect of endothelial stimulation with acetylcholine was assessed and compared with that of endothelial independent vasodilation with nitroglycerin. Both drugs were infused into the main renal artery. Renal artery cross-sectional area was measured with intravascular ultrasound and renal blood flow velocity with the aid of an intravascular Doppler technique.
  
  
  RESULTS
  Both drugs caused a significant and comparable increase in renal artery cross-sectional area (maximal increase [mean +/- SE] 14 +/- 5% with acetylcholine, 15 +/- 5% with nitroglycerin; both changes < 0.05 vs. baseline). Acetylcholine also caused a significant reduction in renal vascular resistance (maximal reduction 55+/- 6%) and increase in renal blood flow (maximal increase 136 +/- 54%). In contrast, nitroglycerin administration showed no significant effect on renal vascular resistance and blood flow.
  
  
  CONCLUSIONS
  Stimulation of endothelium-derived nitric oxide with acetylcholine results in a significant vasodilatory effect on both conductance and resistance renal blood vessels and leads to a marked reduction in renal vascular resistance and enhancement of renal blood blow. Nitroglycerin, an exogenous nitric oxide donor, caused a selective vasodilatory effect on renal conductance but not on resistance blood vessels and failed to increase renal blood flow. These data suggest the possibility that stimulation of endogenous nitric oxide production in the kidney could be used as a therapeutic target for enhancement of renal flow in patients with heart failure.
authors: Department of Medicine, Division of Cardiology, University of Southern California School of Medicine, Los Angeles, 90033, USA.
authors: U
authors: U
authors: Elkayam
authors: G
authors: G
authors: Cohen
authors: H
authors: H
authors: Gogia
authors: A
authors: A
authors: Mehra
authors: J V
authors: JV
authors: Johnson
authors: P A
authors: PA
authors: Chandraratna
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000328:Adult; D018592:Cross-Over Studies; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D008297:Male; D009569:Nitric Oxide / Q000502:physiology*; D005996:Nitroglycerin / Q000494:pharmacology*; D012077:Renal Artery / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000502:physiology; D012079:Renal Circulation / Q000187:drug effects* / Q000502:physiology; D014463:Ultrasonography; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D014665:Vasodilator Agents; D009569:Nitric Oxide; D005996:Nitroglycerin; D000109:Acetylcholine