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We began analyzing https://journals.physiology.org/doi/10.1152/ajpcell.2000.278.2.C423, but it redirected us to https://journals.physiology.org/doi/10.1152/ajpcell.2000.278.2.C423. The analysis below is for the second page.

Title[redir]:
Ca2+ activation of heart mitochondrial oxidative phosphorylation: role of the F0/F1-ATPase | American Journal of Physiology-Cell Physiology | American Physiological Society
Description:
Ca2+ has been postulated as a cytosolic second messenger in the regulation of cardiac oxidative phosphorylation. This hypothesis draws support from the well-known effects of Ca2+ on muscle activity, which is stimulated in parallel with the Ca2+-sensitive dehydrogenases (CaDH). The effects of Ca2+ on oxidative phosphorylation were further investigated in isolated porcine heart mitochondria at the level of metabolic driving force (NADH or Δψ) and ATP production rates (flow). The resulting force-flow (F-F) relationships permitted the analysis of Ca2+ effects on several putative control points within oxidative phosphorylation, simultaneously. The F-F relationships resulting from additions of carbon substrates alone provided a model of pure CaDH activation. Comparing this curve with variable Ca2+ concentration ([Ca2+]) effects revealed an approximate twofold higher ATP production rate than could be explained by a simple increase in NADH or Δψ via CaDH activation. The half-maximal effect of Ca2+ at state 3 was 157 nM and was completely inhibited by ruthenium red (1 μM), indicating matrix dependence of the Ca2+ effect. Arsenate was used as a probe to differentiate between F0/F1-ATPase and adenylate translocase activity by a futile recycling of ADP-arsenate within the matrix, catalyzed by the F0/F1-ATPase. Ca2+increased the ADP arsenylation rate more than twofold, suggesting a direct effect on the F0/F1-ATPase. These results suggest that Ca2+ activates cardiac aerobic respiration at the level of both the CaDH and F0/F1-ATPase. This type of parallel control of both intermediary metabolism and ATP synthesis may provide a mechanism of altering ATP production rates with minimal changes in the high-energy intermediates as observed in vivo.

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🌟 Strong Traffic: 100k - 200k visitors per month


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Keywords {🔍}

atp, nadh, mitochondria, state, mitochondrial, ffatpase, production, mvo, cadh, fig, effects, respiration, data, activation, rate, adp, heart, cytochrome, buffer, work, rates, succinate, table, matrix, substrate, cases, driving, control, substrates, concentration, synthesis, studies, oxygen, determined, conditions, ant, journal, phosphorylation, cytosolic, results, increasing, addition, absence, presented, significant, uncoupling, american, oxidative, force, carbon,

Topics {✒️}

single-factor-dependent variable t-test c423 sections pdf ca2+revealed michaelis-menten kinetics illustrating f0/f1-atpase dependence tailor-made program written carboxy-2′-7′-dichlorofluoresceindiacetate succinimidyl ester luciferin/luciferase luminescent assays external fiber-optic bundle maximal adp-pi-stimulated respiration american physiological society ag-agcl reference electrode modified closed-system respirometer α-chloralose anesthetized animals custom program written marquardt-levenberg algorithm written aps website aps member f0/f1-atpase paul major high-energy intermediate tpp+ ion-selective electrode ion-selective electrode system f0/f1-atpase activity journals quick search effectively short-circuiting ant f0/f1-atpase directly ca2+ dose-response curves f0/f1-atpase increased download figuredownload powerpoint metabolism american journal high-impedance ph meter f0/f1-atpase activation adp-pi-driven rate physiological genomics journal adp-pi-driven respiration l-type ca2+ channels track time-averaged [ca2+] ca2+-stimulated coupled respiration applied physiology journal major rate-limiting step ca2+-stimulated atp production binding-corrected membrane potential physiology-cell physiologyvol limited information ca2+stimulates cadh activity dose-response curves fccp-uncoupled respiration decreased f0/f1-atpase aso4-stimulated mitochondria resulted major driving force physiological [ca2+] activates

Questions {❓}

  • Despite the similarities with whole heart data, the question remains, are changes in the [Ca2+]c with workload adequate to modify mitochondrial metabolism?

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