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Am J Physiol Heart Circ Physiol (July 26, 2002). doi:10.1152/ajpheart.00865.2001
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Articles in PresS, published online ahead of print July 26, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00865.2001
Submitted on October 4, 2001
Accepted on July 19, 2002

Mitochondria Ca2+ uptake is important over a low [Ca2+]i range in arterial smooth muscle

Tomoko Kamishima1* and John M. Quayle1

1 Human Anatomy & Cell Biology, University of Liverpool, Liverpool, Merseyside, United Kingdom

* To whom correspondence should be addressed. E-mail: kamishi{at}liv.ac.uk.

Mitochondrial Ca2+ uptake is usually thought to occur only when intracellular Ca2+ concentration ([Ca2+]i) is high. We investigated whether mitochondrial Ca2+ removal participates in shaping [Ca2+]i signals in arterial smooth muscle over a low [Ca2+]i range. [Ca2+]i was measured using Fura-2 loaded, voltage-clamped cells from rat femoral arteries. Both diazoxide and carbonyl cyanide m-chlorophenylhydrazone (CCCP) depolarized mitochondria. Diazoxide application increased resting [Ca2+]i suggesting Ca2+ is sequestered in mitochondria. Over a low [Ca2+]i range, diazoxide and CCCP slowed Ca2+ removal rate determined following a brief depolarization. When [Ca2+]i was measured during sustained depolarization to -30 mV, CCCP application increased [Ca2+]i. When Ca2+ transients were repeatedly evoked by caffeine applications, CCCP application elevated resting [Ca2+]i. Caffeine-induced Ca2+ transients were compared before and after CCCP application using t1/2 (half decay time, time required to reduce increase in [Ca2+]i by 50 %). CCCP treatment significantly increased t1/2. These results suggest that Ca2+ removal to mitochondria in arterial smooth muscle cells may be important at a low [Ca2+]i.




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