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Respiratory control in the glucose perfused heart
Author(s) -
Katz Lawrence A.,
Koretsky Alan P.,
Balaban Robert S.
Publication year - 1987
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(87)80939-0
Subject(s) - nad+ kinase , creatine , respiration , adenosine triphosphate , pi , adenosine diphosphate , mitochondrion , phosphate , biochemistry , in vivo , phosphocreatine , chemistry , biology , medicine , endocrinology , enzyme , energy metabolism , anatomy , platelet , platelet aggregation , microbiology and biotechnology
The phosphate metabolises, adenosine diphosphate (ADP), inorganic phosphate (P i ), and adenosine triphosphate (ATP), are potentially important regulators of mitochondrial respiration in vivo. However, previous studies on the heart in vivo and in vitro have not consistently demonstrated an appropriate correlation between the concentration of these phosphate metabolites and moderate changes in work and respiration. Recently, mitochondrial NAD(P)H levels have been proposed as a potential regulator of cardiac respiration during alterations in work output. In order to understand better the mechanism of respiratory control under these conditions, we investigated the relationship between the phosphate metabolites, the NAD(P)H levels, and oxygen consumption (Q 02 ) in the isovolumic perfused rat heart during alterations in work output with pacing. ATP, creatine phosphate (CrP), P i and intracellular pH were measured using 31 P NMR. Mitochondrial NAD(P)H levels were monitored using spectrofluorometric techniques. Utilizing glucose as the sole substrate, an increase in paced heart rate led to an increase in Q 02 from 1.73 ± 0.09 to 2.29 ± 0.12 mmol Q 2 /h per g dry wt. No significant changes in the levels of P i , PCr, ATP, or the calculated ADP levels were detected. Under identical conditions, an increase in heart rate was associated with a 23±3% increase in NAD(P)H fluorescence. Thus, under the conditions of these studies, an increase in Q 02 was not associated with an increase in ADP or P i . In contrast, increases in Q 02 were associated with an increase in NAD(P)H. These data are consistent with the notion that increases in the mitochondrial NADH redox state regulate steady‐state levels of respiration when myocardial work is increased.