Mechanisms of blunted muscle vasodilation during peripheral chemoreceptor stimulation in heart failure patients.
We described recently that systemic hypoxia provokes vasoconstriction in heart failure (HF) patients. We hypothesized that either the exaggerated muscle sympathetic nerve activity and/or endothelial dysfunction mediate the blunted vasodilatation during hypoxia in HF patients. Twenty-seven HF patients and 23 age-matched controls were studied. Muscle sympathetic nerve activity was assessed by microneurography and forearm blood flow (FBF) by venous occlusion plethysmography. Peripheral chemoreflex control was evaluated through the inhaling of a hypoxic gas mixture (10% O(2) and 90% N(2)). Basal muscle sympathetic nerve activity was greater and basal FBF was lower in HF patients versus controls. During hypoxia, muscle sympathetic nerve activity responses were greater in HF patients, and forearm vasodilatation in HF was blunted versus controls. Phentolamine increased FBF responses in both groups, but the increase was lower in HF patients. Phentolamine and N(G)-monomethyl-l-arginine infusion did not change FBF responses in HF but markedly blunted the vasodilatation in controls. FBF responses to hypoxia in the presence of vitamin C were unchanged and remained lower in HF patients versus controls. In conclusion, muscle vasoconstriction in response to hypoxia in HF patients is attributed to exaggerated reflex sympathetic nerve activation and blunted endothelial function (NO activity). We were unable to identify a role for oxidative stress in these studies.
Heart Institute, University of São Paulo, São Paulo, Brazil.
Maria Janieire
MJ
Nazaré Nunes Alves
M J N N
MJ
Alves
Marcelo Rodrigues
MR
dos Santos
Thais Simões
TS
Nobre
Daniel Godoy
DG
Martinez
D G
DG
Martinez
Antonio Carlos
AC
Pereira Barretto
Patricia Chakur
PC
Brum
Maria Urbana P B
MU
Rondon
Holly R
HR
Middlekauff
Carlos Eduardo
CE
Negrão
D000328:Adult; D001205:Ascorbic Acid / Q000494:pharmacology; D016022:Case-Control Studies; D002628:Chemoreceptor Cells / Q000502:physiology*; D005542:Forearm / Q000098:blood supply; D006333:Heart Failure / Q000473:pathology* / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000294:innervation* / Q000502:physiology*; D018384:Oxidative Stress / Q000502:physiology; D010646:Phentolamine / Q000494:pharmacology; D012039:Regional Blood Flow / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D019323:omega-N-Methylarginine / Q000494:pharmacology
D019323:omega-N-Methylarginine; D001205:Ascorbic Acid; D010646:Phentolamine