Paradoxical decrease in circulating neuropeptide Y-like immunoreactivity during mild orthostatic stress in subjects with and without congestive heart failure.

Neuropeptide Y (NPY) is thought to be co-released with catecholamines in response to major cardiovascular stresses, but its relation to the release of catecholamines in response to minor stresses has been less well described. We therefore studied the response of plasma NPY-like immunoreactivity (NPY-Li) levels to standing (10 min) in eight normal subjects and 11 patients with congestive heart failure, and to short-term (6h) vasodilator therapy in 13 patients with congestive heart failure. In both normal and heart failure patients, NPY-Li-decreased (296 +/- 73 to 233 +/- 63 pg.ml-1 and 652 +/- 36 to 516 +/- 25 pg.ml-1 (P < 0.01) respectively) in response to standing, whereas catecholamines increased in both groups (norepinephrine 203 +/- 73 to 507 +/- 165 pg.ml-1 and 493 +/- 197 to 813 +/- 336 pg.ml-1 (P < 0.001) respectively and epinephrine 23 +/- 12 to 38 +/- 12 pg.ml-1 and 46 +/- 19 to 62 +/- 28 pg.ml-1 (P < 0.001) respectively). Both basal circulating NPY-Li and catecholamine levels were markedly increased in congestive heart failure patients, but catecholamines and NPY-Li did not correlate with each other. After 6 h of nitroglycerin infusion, mean arterial pressure was decreased, but circulating neurohumoral levels remained unchanged and NPY-Li levels decreased (653 +/- 37 to 517 +/- 26 pg.ml-1, P < 0.01). It is concluded that basal circulating NPY-Li and catecholamine levels are increased in congestive heart failure and that this neurohormone could play a concomitant role in the increase in peripheral resistance in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)