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31 P‐NMR studies of respiratory regulation in the intact myocardium
Author(s) -
From Arthur H.L.,
Petein Marc A.,
Michurski Steven P.,
Zimmer Stevan D.,
Uǧurbil Kâmil
Publication year - 1986
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(86)80992-9
Subject(s) - oxidative phosphorylation , respiration , substrate (aquarium) , perfusion , mitochondrion , phosphate , oxygen , cellular respiration , chemistry , atp synthase , biochemistry , phosphorylation , adenosine triphosphate , respiratory system , biophysics , biology , medicine , enzyme , anatomy , ecology , organic chemistry
The mechanism by which mitochondrial respiration is coupled to ATP consumption in intact tissues is unclear. We determined the relationship between high‐energy phosphate levels and oxygen consumption rate in rat hearts operating over a range of workloads and perfused with different substrates. With pyruvate + glucose perfusion, ADP levels were in general very low, and varied with MVO 2 yielding an apparent K m of 25 ± 5 μM, suggesting regulation of oxidative phosphorylation through availability of ADP. In contrast, with glucose perfusion in the presence or absence of insulin, ADP levels, ADP/ATP ratio or the phosphate potential were relatively constant over the workload range examined and generally not correlated with alterations in MVO 2 ; it is suggested that under these conditions, carbon substrate delivery to the mitochondria may control mitochondrial respiration. The common feature of both of the suggested regulatory mechanisms is substrate limitation which, however, is exercised at different metabolic points depending on the carbon substrate available to the myocardium.