NADPH oxidase-derived reactive oxygen species in skeletal muscle modulates the exercise pressor reflex

Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska Submitted 11 March 2009 ; accepted in final form 2 June 2009 Muscle metabolic by-products during exercise, such as K + , lactic acid, ATP, H + , and phosphate, are well established to be involve...

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Bibliographic Details
Published in:Journal of applied physiology (1985) 2009-08, Vol.107 (2), p.450-459
Main Authors: Wang, Han-Jun, Pan, Yan-Xia, Wang, Wei-Zhong, Zucker, Irving H, Wang, Wei
Format: Article
Language:English
Subjects:
Animals
Antioxidants - administration & dosage
Baroreflex - drug effects
Biological and medical sciences
Blood pressure
Blood Pressure - drug effects
Decerebrate State
Dose-Response Relationship, Drug
Electric Stimulation
Enzyme Inhibitors - administration & dosage
Exercise
Fundamental and applied biological sciences. Psychology
Heart Rate
Hindlimb
Infusions, Intra-Arterial
Male
Models, Animal
Muscle Contraction
Muscle, Skeletal - blood supply
Muscle, Skeletal - drug effects
Muscle, Skeletal - enzymology
Muscle, Skeletal - innervation
Musculoskeletal system
NADPH Oxidases - antagonists & inhibitors
NADPH Oxidases - metabolism
Neurons, Afferent - physiology
Oxidation-Reduction
Oxygen
Physical Exertion
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species - metabolism
Regional Blood Flow
Rodents
Superoxide Dismutase - antagonists & inhibitors
Superoxide Dismutase - metabolism
Time Factors
Xanthine Oxidase - antagonists & inhibitors
Xanthine Oxidase - metabolism
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Summary:Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska Submitted 11 March 2009 ; accepted in final form 2 June 2009 Muscle metabolic by-products during exercise, such as K + , lactic acid, ATP, H + , and phosphate, are well established to be involved in the reflex cardiovascular response to static muscle contraction. However, the role of muscle reactive oxygen species (ROS), a metabolic by-product during muscle contraction, in the exercise pressor reflex (EPR) has not been investigated in detail. In the present study, we evaluated the role of muscle ROS in the EPR in a decerebrate rat model. We hypothesized that muscle NADPH oxidase-derived ROS contributes to sensitization of the EPR. Thus the rise in blood pressure and heart rate in response to a 30-s static contraction induced by electrical stimulation of L 4 /L 5 ventral roots was compared before and after hindlimb arterial infusion of the redox agents: diethyldithiocarbamate, a superoxide dismutase inhibitor; the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethyl piperidine 1-oxyl (tempol); the free radical scavenger dimethylthiourea; a NADPH oxidase inhibitor, apocynin; and a xanthine oxidase inhibitor, allopurinol. The EPR-induced pressor response was augmented after treatment with diethyldithiocarbamate and was attenuated after treatment with tempol, dimethylthiourea, and apocynin. Treatment with allopurinol did not affect the EPR function. None of the drug's affected the EPR heart rate response. In addition, neither the pressor response to electrical stimulation of the central end of dorsal roots, nor femoral blood flow was affected by any treatment. These data suggest that NADPH oxidase-derived muscle ROS plays an excitatory role in the EPR control of blood pressure. static contraction; sympathetic outflow; blood pressure; decerebration Address for reprint requests and other correspondence: W. Wang, Dept. of Cellular and Integrative Physiology, Univ. of Nebraska Medical Center, Omaha, NE 68198-5850 (e-mail: weiwang{at}unmc.edu )
ISSN:8750-7587
1522-1601
DOI:10.1152/japplphysiol.00262.2009