Document Detail


Functional role of peripheral opioid receptors in the regulation of cardiac spinal afferent nerve activity during myocardial ischemia.
MedLine Citation:
PMID:  23645463     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Thinly myelinated Aδ-fiber and unmyelinated C-fiber cardiac sympathetic (spinal) sensory nerve fibers are activated during myocardial ischemia to transmit the sensation of angina pectoris. Although recent observations showed that myocardial ischemia increases the concentrations of opioid peptides and that the stimulation of peripheral opioid receptors inhibits chemically induced visceral and somatic nociception, the role of opioids in cardiac spinal afferent signaling during myocardial ischemia has not been studied. The present study tested the hypothesis that peripheral opioid receptors modulate cardiac spinal afferent nerve activity during myocardial ischemia by suppressing the responses of cardiac afferent nerve to ischemic mediators like bradykinin and extracellular ATP. The nerve activity of single unit cardiac afferents was recorded from the left sympathetic chain (T₂-T₅) in anesthetized cats. Forty-three ischemically sensitive afferent nerves (conduction velocity: 0.32-3.90 m/s) with receptive fields in the left and right ventricles were identified. The responses of these afferent nerves to repeat ischemia or ischemic mediators were further studied in the following protocols. First, epicardial administration of naloxone (8 μmol), a nonselective opioid receptor antagonist, enhanced the responses of eight cardiac afferent nerves to recurrent myocardial ischemia by 62%, whereas epicardial application of vehicle (PBS) did not alter the responses of seven other cardiac afferent nerves to ischemia. Second, naloxone applied to the epicardial surface facilitated the responses of seven cardiac afferent nerves to epicardial ATP by 76%. Third, administration of naloxone enhanced the responses of seven other afferent nerves to bradykinin by 85%. In contrast, in the absence of naloxone, cardiac afferent nerves consistently responded to repeated application of ATP (n = 7) or bradykinin (n = 7). These data suggest that peripheral opioid peptides suppress the responses of cardiac sympathetic afferent nerves to myocardial ischemia and ischemic mediators like ATP and bradykinin.
Authors:
Liang-Wu Fu; John C Longhurst
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2013-05-03
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  305     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2013 Jul 
Date Detail:
Created Date:  2013-07-02     Completed Date:  2013-09-12     Revised Date:  2014-07-01    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H76-85     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Action Potentials / drug effects
Adenosine Triphosphate / pharmacology
Afferent Pathways / drug effects,  metabolism,  physiopathology
Animals
Bradykinin / pharmacology
Cats
Heart Ventricles / innervation*
Myocardial Ischemia / metabolism,  physiopathology*
Naloxone / pharmacology
Narcotic Antagonists / pharmacology
Neural Conduction / drug effects*
Receptors, Opioid / antagonists & inhibitors*
Spinal Nerves / drug effects,  metabolism,  physiopathology*
Grant Support
ID/Acronym/Agency:
HL-66217/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Narcotic Antagonists; 0/Receptors, Opioid; 36B82AMQ7N/Naloxone; 8L70Q75FXE/Adenosine Triphosphate; S8TIM42R2W/Bradykinin
Comments/Corrections

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