Plasmalemmal K(ATP) channels shape triggered calcium transients in metabolically impaired rat atrial myocytes

The relative role of plasmalemmal and mitochondrial ATP-sensitive K+ (KATP) channels in calcium homeostasis of the atrium is little understood. Electrically triggered (1 Hz) cytoplasmic calcium transients were measured by 340-to-380-nm wavelength fura 2 emission ratios in cultured rat atrial myocyte...

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Bibliographic Details
Published in:American journal of physiology. Heart and circulatory physiology 2002-12, Vol.52 (6), p.H2296
Main Authors: Baumann, Philippe, Poitry, Serge, Roatti, Angela, Baertschi, Alex J
Format: Article
Language:English
Subjects:
Anatomy & physiology
Calcium
Metabolism
Rodents
Online Access:Get full text
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Summary:The relative role of plasmalemmal and mitochondrial ATP-sensitive K+ (KATP) channels in calcium homeostasis of the atrium is little understood. Electrically triggered (1 Hz) cytoplasmic calcium transients were measured by 340-to-380-nm wavelength fura 2 emission ratios in cultured rat atrial myocytes. CCCP, a mitochondrial protonophore (100-400 nmol/l), dose dependently reduced the transient amplitude by up to 85%, caused a slow rise in baseline calcium, and reduced the recovery time constant of the transient from 143 to 91 ms (P < 0.05). However, neither 5-hydroxydecanoate, a mitochondrial KATP channel blocker, nor diazoxide (500 µmol/l) affected the amplitude, baseline, or time constant in CCCP-treated cells. HMR-1098 (30 µmol/l), a plasmalemmal KATP channel blocker, and glibenclamide (1 mumol/l) increased the amplitude in CCCP-treated myocytes by 69-82%, sharply elevated the calcium baseline, and prolonged the recovery time constant to 181-193 ms (P < 0.01). Thus opening of plasmalemmal but not mitochondrial KATP channels reduces the calcium overload in metabolically compromised but otherwise intact atrial myocytes. Mitochondrial KATP channels probably operate through a different mechanism to afford ischemic protection.
ISSN:0363-6135
1522-1539