Lack of inotropic effects of neuropeptide Y in human myocardium.
The sympathetic co-transmitter neuropeptide Y (NPY) inhibits cardiac contractility in vivo in the rat heart. We tested whether NPY alters the force of contraction or the activity of adenylate cyclase in the isolated human right atrium. Neuropeptide Y did not affect basal-or isoproterenol-stimulated force of contraction and did not inhibit forskolin-stimulated adenylate cyclase activity. We conclude that NPY does not directly decrease cardiac contractility in humans. The inhibitory cardiac effects of NPY are likely to be secondary to coronary vasoconstriction, presynaptic inhibition of catecholamine release, and/or baroreflex activity.
Michel
M C
MC
Department of Pharmacology, University of California San Diego, La Jolla.
Wirth
S C
SC
Zerkowski
H R
HR
Maisel
A S
AS
Motulsky
H J
HJ
D000242:Cyclic AMP / Q000378:metabolism; D003864:Depression, Chemical; D006321:Heart / Q000187:drug effects*; D006801:Humans; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism; D009478:Neuropeptide Y / Q000494:pharmacology*
D009478:Neuropeptide Y; D000242:Cyclic AMP; D007545:Isoproterenol