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Department of Human Anatomy and Cell Biology, University of Liverpool, Liverpool L69 3GE, United Kingdom
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 the mitochondria. Diazoxide application increased resting [Ca2+]i, suggesting that
Ca2+ is sequestered in mitochondria. Over a low
[Ca2+]i range, diazoxide and CCCP slowed
Ca2+ removal rate, determined after 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 the half decay time, or time required to reduce
increase in [Ca2+]i by 50%
(t1/2). 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.
carbonyl cyanide m-chlorophenylhydrazone; diazoxide; fura 2; rhodamine 123; sarcoplasmic reticulum
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