Venous neuropeptide Y receptor responsiveness in patients with chronic heart failure.
BACKGROUND
Chronic heart failure is associated with increased sympathetic nerve activity and elevated plasma neuropeptide Y levels. The aim of this study was to investigate whether increased neuropeptide Y release altered vascular neuropeptide Y responses in the dorsal hand veins in patients with chronic heart failure.


RESULTS
Neuropeptide Y responsiveness was studied in vivo with use of a hand vein tonometry technique in 14 patients with chronic heart failure and left ventricular ejection fraction (LVEF) values <20%, 16 patients with LVEF values from 20% to 35%, and 16 age-similar healthy control subjects. Plasma norepinephrine and neuropeptide Y levels were significantly elevated in patients with chronic heart failure and LVEF values <20% compared with control subjects (P < .01). Plasma neuropeptide Y but not norepinephrine levels were significantly elevated in patients with chronic heart failure and LVEF values from 20% to 35% compared with control subjects (P < .01). Increasing doses of neuropeptide Y (25 to 2,000 pmol/min) were infused into a dorsal hand vein of each subject. Dose-dependent venoconstriction to neuropeptide Y was observed in all subjects studied. The neuropeptide Y dose-response curve in patients with LVEF values from 20% to 35% was significantly shifted to the left compared with patients with LVEF values <20% and control subjects (P < .01), whereas no significant difference was observed between the control subjects and the patients with LVEF values <20%. No significant difference in neuropeptide Y dose responses was observed between patients with chronic heart failure with plasma neuropeptide Y levels above the median and patients with chronic heart failure with plasma neuropeptide Y levels below the median.


CONCLUSIONS
In vivo venous neuropeptide Y receptor responsiveness is increased in patients with chronic heart failure and LVEF values from 20% to 35%. This increased neuropeptide Y responsiveness may contribute to venoconstriction at this stage of heart failure.
Feng
Q
Q
Department of Medicine, London Health Sciences Centre, University of Western Ontario, Canada.
Lambert
M L
ML
Callow
I D
ID
Arnold
J M
JM
D002303:Cardiac Output, Low / Q000097:blood* / Q000503:physiopathology; D016022:Case-Control Studies; D002908:Chronic Disease; D004305:Dose-Response Relationship, Drug; D005260:Female; D006225:Hand / Q000098:blood supply; D006801:Humans; D008297:Male; D008875:Middle Aged; D009478:Neuropeptide Y / Q000008:administration & dosage*; D011863:Radioimmunoassay; D017476:Receptors, Neuropeptide Y / Q000097:blood*; D013318:Stroke Volume; D014065:Tonometry, Ocular; D014680:Veins
D009478:Neuropeptide Y; D017476:Receptors, Neuropeptide Y