Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-5-8
pubmed:abstractText
Although recent studies have reported hypocretin 1 (hcrt-1)-like-immunoreactivity (ir) within the region of the nucleus ambiguus (Amb) in the caudal brain stem, the function of hcrt-1 in the Amb on cardiovascular function is not known. Three series of experiments were done in male Wistar rats to investigate the effects of microinjections of hcrt-1 into Amb on heart rate (HR), mean arterial pressure (MAP), and the arterial baroreceptor reflex. In the first series, a detailed mapping of the distribution of hcrt-1- and hcrt-1 receptor (hcrtR-1)-like-ir was obtained of the Amb region. Although hcrt-1-like- and hcrtR-1-like-ir were found throughout the rostrocaudal extent of the Amb and adjacent ventrolateral medullary reticular formation, most of the hcrtR-1-like-ir was observed in the area just ventral to the compact formation of Amb, in the region of the external formation of the nucleus (Ambe). In the second series, the Amb region that contained hcrt-1 and hcrtR-1-ir was explored for sites that elicited changes in HR and MAP in urethane and alpha-chloralose-anesthetized rats. Microinjections of hcrt-1 (0.5-2.5 pmol) into the Ambe elicited a dose-related decrease in HR, with little or no direct change in MAP. The small decreases in MAP were found to be secondary to the HR changes. The largest bradycardia responses were elicited from sites in the Ambe. Administration (iv) of the muscarinic receptor antagonist atropine methyl bromide or ipsilateral vagotomy abolished the HR response, indicating that the HR response was due to activation of vagal cardiomotor neurons. In the final series, microinjections of hcrt-1 into the Ambe significantly potentiated the reflex bradycardia elicited by activation of the baroreflex as a result of the increased MAP after the intravenous injection of phenylephrine. These data suggest that hcrt-1 in the Ambe activates neuronal systems that alter the excitability of central circuits that reflexly control the circulation through the activation of vagal preganglionic cardioinhibitory neurons.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0363-6119
pubmed:author
pubmed:issnType
Print
pubmed:volume
284
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R1611-20
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12573979-Animals, pubmed-meshheading:12573979-Autonomic Nervous System, pubmed-meshheading:12573979-Blood Pressure, pubmed-meshheading:12573979-Bradycardia, pubmed-meshheading:12573979-Brain Stem, pubmed-meshheading:12573979-Carrier Proteins, pubmed-meshheading:12573979-Dose-Response Relationship, Drug, pubmed-meshheading:12573979-Heart, pubmed-meshheading:12573979-Heart Rate, pubmed-meshheading:12573979-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:12573979-Male, pubmed-meshheading:12573979-Muscarinic Antagonists, pubmed-meshheading:12573979-Neuropeptides, pubmed-meshheading:12573979-Rats, pubmed-meshheading:12573979-Rats, Wistar, pubmed-meshheading:12573979-Receptors, G-Protein-Coupled, pubmed-meshheading:12573979-Receptors, Muscarinic, pubmed-meshheading:12573979-Receptors, Neuropeptide, pubmed-meshheading:12573979-Vagus Nerve
pubmed:year
2003
pubmed:articleTitle
Cardiac effects of hypocretin-1 in nucleus ambiguus.
pubmed:affiliation
Department of Physiology and Pharmacology, Faculty of Medicine and Dentistry, Health Sciences Centre, University of Western Ontario, London, Ontario, Canada N6A 5C1. john.ciriello@fmd.uwo.ca
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't