Plasmalemmal KATP channels shape triggered calcium transients in metabolically impaired rat atrial myocytes.

The relative role of plasmalemmal and mitochondrial ATP-sensitive K(+) (K(ATP)) 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 K(ATP) channel blocker, nor diazoxide (500 micromol/l) affected the amplitude, baseline, or time constant in CCCP-treated cells. HMR-1098 (30 micromol/l), a plasmalemmal K(ATP) channel blocker, and glibenclamide (1 micromol/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 K(ATP) channels reduces the calcium overload in metabolically compromised but otherwise intact atrial myocytes. Mitochondrial K(ATP) channels probably operate through a different mechanism to afford ischemic protection.