The aim of this study was to investigate neuropeptide Y (NPY)-induced vasoconstrictions in rat blood vessels and which NPY receptor subtype is involved in vasoconstrictions. NPY produced marked contractions in rat common jugular, brachial, portal, femoral and tail veins, and vena cava inferior, whereas it produced little or no contractions in rat common carotid, brachial, femoral and tail arteries, and thoracic and abdominal aortae. The maximal NPY-induced contractions were larger than maximal phenylephrine (PE)-induced contractions in the veins. These NPY-induced contractions were blocked by the Y1 antagonists, SRL-21, and BIBP3226 but not by the Y5 antagonist, L-152804. A Y2 agonist, NPY (13-36), did not produce contractions. RT-PCR showed that NPY-Y1 was the only receptor subtype in the veins indicating that NPY-induced contractions are mediated through the Y1 receptor. Pretreatment with NPY showed a rapid and long-lasting desensitization of these contractions. The marked NPY-induced contractions and its desensitization in the veins suggest the physiological relevance of NPY in the venous circulation.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s1537-1891(03)00044-2 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Neuropeptide Y (NPY) inhibits spontaneous contraction of the mouse atrium by possible activation of the NPY1 receptor.
Auton Autacoid Pharmacol
March 2017
Department of Veterinary Medicine, Rakuno Gakuen University, Ebetsu, Hokkaido, Japan.
Neuropeptide Y (NPY) causes various central and peripheral actions through activation of G-protein-coupled NPY receptors. Although a species-dependent difference in cardiac actions of NPY has been reported, the responses to NPY have not been examined in mice, widely used experimental animals. This study aimed to clarify the responses to NPY and the receptor subtype involved in the responses in mouse atrium.
View Article and Find Full Text PDFEndogenous peptide YY and neuropeptide Y inhibit colonic ion transport, contractility and transit differentially via Y₁ and Y₂ receptors.
Br J Pharmacol
September 2011
King's College London, Wolfson Centre for Age-Related Diseases, Guy's Campus, London, UK.
Background And Purpose: Peptide YY (PYY) and neuropeptide Y (NPY) activate Y receptors, targets under consideration as treatments for diarrhoea and other intestinal disorders. We investigated the gastrointestinal consequences of selective PYY or NPY ablation on mucosal ion transport, smooth muscle activity and transit using wild-type, single and double peptide knockout mice, comparing mucosal responses with those from human colon.
Experimental Approach: Mucosae were pretreated with a Y₁ (BIBO3304) or Y₂ (BIIE0246) receptor antagonist and changes in short-circuit current recorded.
Marked neuropeptide Y-induced contractions via NPY-Y1 receptor and its desensitization in rat veins.
Vascul Pharmacol
December 2002
Division of Pharmacology, Department of Molecular Genetics and Signal Transduction Research, Course for Molecular and Cellular Medicine, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Niigata, 951-8510, Japan.
The aim of this study was to investigate neuropeptide Y (NPY)-induced vasoconstrictions in rat blood vessels and which NPY receptor subtype is involved in vasoconstrictions. NPY produced marked contractions in rat common jugular, brachial, portal, femoral and tail veins, and vena cava inferior, whereas it produced little or no contractions in rat common carotid, brachial, femoral and tail arteries, and thoracic and abdominal aortae. The maximal NPY-induced contractions were larger than maximal phenylephrine (PE)-induced contractions in the veins.
View Article and Find Full Text PDFEffect of neuropeptide Y on the sympathetic contraction of the rabbit central ear artery during cooling.
Pflugers Arch
August 2000
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Madrid, Spain.
In order to analyse the effect of neuropeptide Y (NPY) on the cutaneous vascular response to sympathetic nerve stimulation during cooling, the isometric response of isolated 2-mm segments of the rabbit central ear (cutaneous) artery was recorded at 37 degrees C and during cooling (30 degrees C). Electrical field stimulation (4-16 Hz) at 37 degrees C produced a frequency-dependent contraction, which was reduced during cooling (45% for 16 Hz) and potentiated by NPY (10(-8), 3x10(-8) and 10(-7) M), this potentiation being greater at 30 degrees C than at 37 degrees C. The NPY-induced potentiation of the contraction elicited by electrical field stimulation (8 Hz) was abolished by an antagonist of Y1 subtype NPY receptors, BIBP3226 (10(-6) M), at 37 degrees C and 30 degrees C, reduced by phentolamine (10(-6) M) at 30 degrees C but not at 37 degrees C, was not modified by the purinoceptor antagonist PPADS (3x10(-5) M) and was reduced by application of both phentolamine and PPADS at both temperatures.
View Article and Find Full Text PDFPregnancy is associated with altered response to neuropeptide Y in uterine artery.
Mol Hum Reprod
April 2000
Tayside Institute of Child Health, University of Dundee, Ninewells Hospital & Medical School, Dundee, DD1 9SY, Scotland, UK.
Pregnancy is associated with a significant increase in uterine blood flow which contributes to optimal fetal development. Although neuropeptide Y (NPY) is considered to be an important regulator of uterine blood flow, it is not known whether: (i) products from the vascular endothelium modulate NPY action in the uterine artery; (ii) pregnancy changes the responsiveness of the uterine artery to NPY, or (iii) NPY interacts with noradrenaline and acetylcholine on the uterine artery, with pregnancy regulating this possible interaction. In the present study, NPY induced a concentration-dependent contraction of guinea pig uterine arterial rings both intact and denuded of endothelium.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!