Al Nasser, I;
The α-adrenergic-mediated activation of the cardiac mitochondrial Ca uniporter and its role in the control of intramitochondrial Ca in vivo.
333 - 342.
Administration of methoxamine (10 μM, 2 min) to perfused rat hearts increased the rate at which subsequently isolated mitochondria accumulated Ca. Methoxamine did not change significantly the development of ΔΨ with time or the basal rates of Ca flux on inhibition of the uniporter with Ruthenium Red. 2. With 200 μM-P(i), the rates of Ca uptake at constant ΔΨ were unaffected by the small variations in endogenous [P(i)] between mitochondrial preparations, and were also unaffected by changes in internal Ca over the approximate range 8-43 nmol of Ca/mg. At low internal Ca (about 8 nmol/mg of protein) the rates of Ca uptake at constant ΔΨ were unaffected by addition of 200 μM-P(i). Under these conditions, the uniporter activity and the uniporter conductance were increased by 38-40% by methoxamine pretreatment. The endogenous Ca content of mitochondria from control heart was about 1.8 nmol of Ca/mg of protein. Perfusion with agonist increased the Ca content as follows: 10 μM-methoxamine (2 min), 48%; 1 μM-isoprenaline (2 min), 100%; 1 μM-adrenaline (2 min), 140%. The implications of the data for the adrenergic control of oxidative metabolisn by intramitochondrial Ca is discussed.
|Title:||The α-adrenergic-mediated activation of the cardiac mitochondrial Ca uniporter and its role in the control of intramitochondrial Ca in vivo|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Life Sciences > Biosciences (Division of)|
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