Key result
Mitochondrial inhibitors abolish high K+-induced Ca++ uptake without affecting the contractile response.
Why the study?
The relationship between mitochondrial Ca++ uptake and potassium-induced tension responses in rabbit aortic smooth muscle was unclear.
The study demonstrates that increased low affinity Ca++ retention elicited by high K+ in rabbit aortic smooth muscle represents mitochondrial Ca++ uptake, which can be dissociated from contractile responses using mitochondrial inhibitors.
Mitochondrial inhibitors dissociate Ca uptake from contraction; leaves open distinct Ca pools in vascular physiology.
Effects of antimycin A, oligomycin and KCN on tension responses to high K+ or NE and on related Ca++ movements were investigated in rabbit aortic smooth muscle. Selected concentrations of antimycin A (10(-6) g/ml), oligomycin (10(-6) g/ml) and KCN (1 mM) had little effect on the K+-induced contractile response even though all three agents abolished the increase in La+++-resistant low affinity Ca++ uptake elicited with high K+. Though the mitochondrial inhibitors had varied effects on the NE-induced contractile response, they had no effect on the NE-induced decrease in La+++-resistant high affinity Ca++. Oxygen consumption of the muscle tissue was decreased by antimycin A or oligomycin. These results suggest that the increase in low affinity Ca++ retention elicited with high K+ represents Ca++ uptake by mitochondria. Thus, the correlation between K+-induced uptake of Ca++ and an increased retention of La+++-resistant low affinity Ca++ after exposure to K+ are sequential events that can be associated by inhibitors of mitochondrial Ca++ uptake.
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Karaki et al. (2008) studied this question. Antimycin A, oligomycin, and KCN was evaluated on Tension responses to high K+ or NE and related Ca++ movements. Antimycin A, oligomycin, and KCN abolished the increase in La+++-resistant low affinity Ca++ uptake elicited with high K+ but had little effect on the K+-induced contractile response.
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