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(The FASEB Journal. 2007;21:979.10)
© 2007 FASEB
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979.10

Intracellular Ca2+ homeostasis by mitochondria and SR in rat intrapulmonary arteries

Silke Becker, Jeremy PT Ward and Philip I Aaronson

Asthma, Allergy and Lung Biology, King’s College London, 2nd Floor Thomas Guy House, London, SE1 9RT, United Kingdom

ABSTRACT

Mitochondria are major intracellular Ca2+ stores and may play a key role in Ca2+ homeostasis. We studied the interaction of SR and mitochondrial Ca2+ release in rat pulmonary arteries (IPA), using rhodamine-123 to estimate mitochondrial membrane potential. Contraction induced by the mitochondrial uncoupler FCCP (0.3 µM) was greatly potentiated by constriction with PGF2{alpha} and was endothelium-dependent. The mitochondrial Na+-Ca2+ exchange blocker CGP-37157 (30 µM) strongly inhibited FCCP-induced contraction, as did inhibition of ryanodine receptors with dantrolene (50 µM), depletion of SR Ca2+ stores with CPA (30 µM), inhibition of voltage-gated Ca2+ channels with diltiazem (10 µM), and voltage-independent Ca2+ channels with 2-APB (75 µM) or SK&F (100 µM). CGP-37157 depolarized mitochondria, suggesting this electrogenic mechanism has a role in Ca2+ uptake. These data suggest mitochondria take up Ca2+ via their Na+-Ca2+ exchanger in IPA. They also indicate that mitochondrial Ca2+ release may trigger release from the SR via ryanodine receptors, so depleting the SR. FCCP also activates Ca2+ influx through voltage-gated Ca2+ channels in smooth muscle and voltage-independent Ca2+ channels in smooth muscle and endothelium.





This Article
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