Sodium nitrate supplementation alters mitochondrial H2O2 emission but does not improve mitochondrial oxidative metabolism in the heart of healthy rats

Autor: Jason S. Huber, Paula M. Miotto, Graham P. Holloway, Luc J. C. van Loon, Cynthia M. F. Monaco, Jeremy A. Simpson
Přispěvatelé: Humane Biologie, RS: NUTRIM - R3 - Respiratory & Age-related Health
Jazyk: angličtina
Rok vydání: 2018
Předmět:
Male
0301 basic medicine
Bioenergetics
Physiology
Hemodynamics
Blood Pressure
BLOOD-PRESSURE
030204 cardiovascular system & hematology
Mitochondrion
bioenergetics
hemodynamics
Mitochondria
Heart
Ventricular Function
Left
Rats
Sprague-Dawley
chemistry.chemical_compound
0302 clinical medicine
XANTHINE OXIDOREDUCTASE
Myocytes
Cardiac
biology
CREATINE-KINASE
HUMAN SKELETAL-MUSCLE
3. Good health
Adenosine Diphosphate
mitochondria
medicine.anatomical_structure
Ventricular pressure
INORGANIC NITRATE
Oxidation-Reduction
Research Article
Signal Transduction
medicine.medical_specialty
Mean arterial pressure
heart
Nitric oxide
KINASE KNOCKOUT MICE
03 medical and health sciences
nitrate
Physiology (medical)
Internal medicine
Ventricular Pressure
medicine
Animals
Nitrates
NITRIC-OXIDE
Skeletal muscle
Hydrogen Peroxide
Myocardial Contraction
OXYGEN-CONSUMPTION
030104 developmental biology
Endocrinology
chemistry
TIME-TRIAL PERFORMANCE
DIETARY NITRATE
Dietary Supplements
biology.protein
Creatine kinase
Energy Metabolism
Zdroj: American Journal of Physiology-regulatory Integrative and Comparative Physiology, 315(2), R191-R204. American Physiological Society
ISSN: 0363-6119
DOI: 10.1152/ajpregu.00275.2017
Popis: Supplementation with dietary inorganic nitrate ([Formula: see text]) is increasingly recognized to confer cardioprotective effects in both healthy and clinical populations. While the mechanism(s) remains ambiguous, in skeletal muscle oral consumption of NaNO3 has been shown to improve mitochondrial efficiency. Whether NaNO3 has similar effects on mitochondria within the heart is unknown. Therefore, we comprehensively investigated the effect of NaNO3 supplementation on in vivo left ventricular (LV) function and mitochondrial bioenergetics. Healthy male Sprague-Dawley rats were supplemented with NaNO3 (1 g/l) in their drinking water for 7 days. Echocardiography and invasive hemodynamics were used to assess LV morphology and function. Blood pressure (BP) was measured by tail-cuff and invasive hemodynamics. Mitochondrial bioenergetics were measured in LV isolated mitochondria and permeabilized muscle fibers by high-resolution respirometry and fluorometry. Nitrate decreased ( P < 0.05) BP, LV end-diastolic pressure, and maximal LV pressure. Rates of LV relaxation (when normalized to mean arterial pressure) tended ( P = 0.13) to be higher with nitrate supplementation. However, nitrate did not alter LV mitochondrial respiration, coupling efficiency, or oxygen affinity in isolated mitochondria or permeabilized muscle fibers. In contrast, nitrate increased ( P < 0.05) the propensity for mitochondrial H2O2 emission in the absence of changes in cellular redox state and decreased the sensitivity of mitochondria to ADP (apparent Km). These results add to the therapeutic potential of nitrate supplementation in cardiovascular diseases and suggest that nitrate may confer these beneficial effects via mitochondrial redox signaling.
Databáze: OpenAIRE
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