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 s tudy was to investigate whether increased neuropeptide Y release altered va scular neuropeptide Y responses in the dorsal hand veins in patients with c hronic heart failure. Methods and results: Neuropeptide Y responsiveness was studied in vivo with use of a hand vein tonometry technique in 14 patients with chronic heart f ailure and left ventricular ejection fraction (LVEF) values <20%, 16 patien ts with LVEF values from 20% to 35%, and 16 age-similar healthy control sub jects. Plasma norepinephrine and neuropeptide Y levels were significantly e levated in patients with chronic heart failure and LVEF values <20% compare d with control subjects (P < .01), Plasma neuropeptide Y but: not norepinep hrine levels were significantly elevated in patients with chronic heart fai lure and LVEP values from 20% to 35% compared with control subjects (P < .0 1), Increasing doses of neuropeptide Y (25 to 2000 pmol/min) were infused i nto a dorsal hand vein of each subject, Dose-dependent venoconstriction to neuropeptide Y was observed. in all subjects studied. The neuropeptide P do se-response curve in patients with LVEP values from 20% to 35% was signific antly shifted to the left compared with patients LVEF values <20% and contr ol subjects (P < .01), whereas no significant difference was observed betwe en the control subjects and the patients with LVEP values <20%. No signific ant difference in neuropeptide Y dose responses was observed between patien ts with chronic heart failure with plasma neuropeptide P levels above: the median and patients with chronic heart failure with plasma neuropeptide Y l evels below the median. Conclusions: In vivo venous neuropeptide Y receptor responsiveness is incre ased in patients with chronic heart failure and LVEF values from 20% to 35% . This increased neuropeptide Y responsiveness may contribute to venoconstr iction at this stage of heart failure.