Stress-induced mesenteric vasoconstriction in rats is mediated by
neuropeptide y-y1 receptors.
Zukowska-Grojec, Zofia, Emmanuel K. Dayao, Ewa Karwatowska-Prokopczuk,
Gabriel J. Hauser, and Henri N. Doods.
Department of Physiology and Biophysics, and Department of
Pediatrics, Georgetown University Medical Center, Washington, D.C.,
U.S.A. and Department of Cardiovascular Pharmacology, Dr. Karl Thomae
GmbH, Biberach, Germany
APStracts 2:0530H, 1995.
The physiological role of neuropeptide Y (NPY), a sympathetic co
-transmitter and a vasoconstrictor, has not been determined yet. For
the first time, we used a specific non-peptide antagonist to the NPY
-Y1 receptor (BIBP3226) to study the involvement of NPY in stress
-induced vasoconstriction in the mesenteric bed. In rats subjected to
cold water stress (COLD), plasma NPY-ir levels increased
progressively from 0.15+.01 to 0.32+0.05 pmol/ml, and remained
elevated during recovery. Administration of BIBP3226 (3 mg/kg/hr
infusion) tended to decrease the stress-induced pressor response and
significantly attenuated the post-COLD elevation of blood pressure.
The COLD-induced fall in the superior mesenteric artery blood flow,
and the increase of up to 300% in the mesenteric vascular resistance
were either reduced or eliminated by BIBP3226. Conversely, the Y1
antagonist had no effect on the COLD-induced tachycardia. This study
provides the first evidence of the physiological role of NPY. The
peptide is released during stress and increases mesenteric vascular
resistance via activation of its Y1 receptors. Specific Y1 receptor
antagonists may therefore be of potential benefit in prevention or
treatment of stress-induced vasospasm.
Received 1 September 1995; accepted in final form 9 November
1995.
APS Manuscript Number H827-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95