Potassium-channel openers — drugs that promote the influx of potassium — might help protect heart cells (myocytes) against damage from heart attack, proposes a study on guinea-pig myocytes, published in the 1 November issue of Science. Brian O'Rourke and colleagues have discovered a new type of potassium channel in the membrane of myocyte mitochondria, and have shown that a drug that opened the channel protected isolated rabbit hearts against tissue death and low oxygen conditions caused by a heart attack.

Despite the great benefits seen in major trials of the use of thrombolytic therapy and various adjunctive treatments, such as beta-blocker therapy and angiotensin-converting enzyme (ACE) inhibitors, ischaemic heart disease and myocardial infarction (heart attacks) remain the largest cause of death in developed countries.

Ions traverse the plasma membrane of cells through channels created by embedded transmembrane proteins, driven by an electrochemical gradient between the extracellular and intracellular contents. Ion channels on the mitochondrial inner membrane similarly mediate ion flow between the cytoplasm and the mitochondrial matrix compartment, and influence myocyte cell function in diverse ways. The mitochondrial ATP-sensitive potassium channel (mitoKATP) has an instrumental role in protecting myocytes from necrotic and apoptotic cell death, whereas other channels contribute to mitochondrial dysfunction. Drugs that block the flow of calcium ions into heart muscle cells, such as verapamil or diltiazem, are known to treat various heart conditions, but a growing body of evidence indicates that encouraging the flow of potassium across certain membranes inside heart muscle cells might be useful as well.

The newly identified mitochondrial potassium channel (mitoKCa) was activated by calcium ions, and had similar properties to the cell-membrane calcium-activated potassium channel. The authors showed that a significant portion of potassium passes through the mitoKCa channel into the mitochondria.

The authors speculate that the function of mitoKCa could be to improve the efficiency of mitochondrial energy production when cellular calcium levels increase, because potassium ions are required for optimal oxidative phosphorylation — a necessity for respiration. Potassium ions might also modulate other mitochondrial functions, such as the production of reactive oxygen species. Although opening mitoKCa protects against ischaemic injury in animal models, it remains to be seen if the same is true in humans.