Intravenous NPY (27-36)-D decreases cardiac output in conscious Sprague-Dawley rats.
Intravenous (IV) administration of NPY (27-36)-D, a substituted carboxyterminal fragment of neuropeptide Y (NPY), decreases mean arterial pressure (MAP) in normo-and hypertensive rats by a mechanism partially involving histamine receptors. The purpose of this study is to further characterize the cardiovascular effects of NPY (27-36)-D. NPY (27-36)-D dose-dependently decreased MAP, cardiac output, and stroke volume without significantly altering peripheral resistance. Myocardial contractility diminished by 151.2 +/- 31.8, 529.6 +/- 182.5, and 495.4 +/- 66.7 mmHg/s2 in rats treated with 300, 500, and 750 nmol/kg NPY (27-36)-D, respectively. Therefore, NPY (27-36)-D modifies MAP, in part, by a reversible negative inotropic effect on the heart.
Roscoe
A K
AK
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, NC 27858, USA.
Nyce
J
J
Wooles
W R
WR
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D002302:Cardiac Output / Q000187:drug effects*; D003243:Consciousness; D004305:Dose-Response Relationship, Drug; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects*; D009478:Neuropeptide Y / Q000031:analogs & derivatives* / Q000138:chemical synthesis / Q000494:pharmacology; D010446:Peptide Fragments / Q000138:chemical synthesis / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D009478:Neuropeptide Y; D010446:Peptide Fragments; C095005:neuropeptide Y (27-36), Tyr(27,36)-Thr(32)-