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Voltage-gated L-type Ca 2+  current ( I Ca,L ) induces contraction of arterial smooth muscle cells (ASMCs), and I Ca,L  is increased by H 2 O 2  in ASMCs. Superoxide released from the mitochondrial respiratory chain (MRC) is dismutated to H 2 O 2 . We studied whether superoxide per se acutely modulates I Ca,L  in ASMCs using cultured A7r5 cells derived from rat aorta. Rotenone is a toxin that inhibits complex I of the MRC and increases mitochondrial superoxide release. The superoxide content of mitochondria was estimated using mitochondrial-specific MitoSOX and HPLC methods, and was shown to be increased by a brief exposure to 10 μM rotenone. I Ca,L  was recorded with 5 mM BAPTA in the pipette solution. Rotenone administration (10 nM to 10 μM) resulted in a greater I Ca,L  increase in a dose-dependent manner to a maximum of 22.1% at 10 μM for 1 min, which gradually decreased to 9% after 5 min. The rotenone-induced I Ca,L  increase was associated with a shift in the current-voltage relationship ( I-V) to a hyperpolarizing direction. DTT administration resulted in a 17.9% increase in I Ca,L  without a negative shift in I–V, and rotenone produced an additional increase with a shift. H 2 O 2  (0.3 mM) inhibited I Ca,L  by 13%, and additional rotenone induced an increase with a negative shift. Sustained treatment with Tempol (4-hydroxy tempo) led to a significant I Ca,L  increase but it inhibited the rotenone-induced increase. Staurosporine, a broad-spectrum protein kinase inhibitor, partially inhibited I Ca,L  and completely suppressed the rotenone-induced increase. Superoxide released from mitochondria affected protein kinases and resulted in stronger I Ca,L  preceding its dismutation to H 2 O 2 . The removal of nitric oxide is a likely mechanism for the increase in I Ca,L .

Rotenone-stimulated superoxide release from mitochondrial complex I acutely augments L-type Ca2+ current in A7r5 aortic smooth muscle cells

Rotenone-stimulated superoxide release from mitochondrial complex I acutely augments L-type Ca²⁺ current in A7r5 aortic smooth muscle cells