Investigation of the mechanisms of cyclooxygenase-mediated mechanoreflex sensitization in a rat model of simulated peripheral artery disease.
Animals
Cyclooxygenase Inhibitors
/ pharmacology
Dinoprostone
/ metabolism
Disease Models, Animal
Femoral Artery
/ physiopathology
Ganglia, Spinal
/ metabolism
Hindlimb
Indomethacin
/ pharmacology
Ligation
Male
Mechanoreceptors
/ metabolism
Mechanotransduction, Cellular
Muscle Contraction
Muscle, Skeletal
/ blood supply
Peripheral Arterial Disease
/ enzymology
Prostaglandin-Endoperoxide Synthases
/ metabolism
Rats, Sprague-Dawley
Receptors, Prostaglandin E, EP4 Subtype
/ metabolism
Receptors, Thromboxane A2, Prostaglandin H2
/ metabolism
Reflex
blood pressure
exercise pressor reflex
muscle afferents
Journal
American journal of physiology. Heart and circulatory physiology
ISSN: 1522-1539
Titre abrégé: Am J Physiol Heart Circ Physiol
Pays: United States
ID NLM: 100901228
Informations de publication
Date de publication:
01 11 2019
01 11 2019
Historique:
pubmed:
31
8
2019
medline:
9
4
2020
entrez:
31
8
2019
Statut:
ppublish
Résumé
Mechanical and metabolic stimuli within contracting skeletal muscles reflexly increase sympathetic nervous system activity and blood pressure. That reflex, termed the exercise pressor reflex, is exaggerated in patients with peripheral artery disease (PAD) and in a rat PAD model with a chronically ligated femoral artery. The cyclooxygenase (COX) pathway contributes to the exaggerated pressor response during rhythmic skeletal muscle contractions in patients with PAD, but the specific mechanism(s) of the COX-mediated exaggeration are not known. In decerebrate, unanesthetized rats with a chronically ligated femoral artery ("ligated" rats), we hypothesized that hindlimb arterial injection of the COX inhibitor indomethacin would reduce the pressor response during 1-Hz dynamic hindlimb skeletal muscle stretch; a model of the activation of the mechanical component of the exercise pressor reflex (i.e., the mechanoreflex). In ligated rats (
Identifiants
pubmed: 31469294
doi: 10.1152/ajpheart.00399.2019
pmc: PMC6879919
doi:
Substances chimiques
Cyclooxygenase Inhibitors
0
Ptger4 protein, rat
0
Receptors, Prostaglandin E, EP4 Subtype
0
Receptors, Thromboxane A2, Prostaglandin H2
0
Prostaglandin-Endoperoxide Synthases
EC 1.14.99.1
Dinoprostone
K7Q1JQR04M
Indomethacin
XXE1CET956
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
H1050-H1061Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL142877
Pays : United States
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