Researchers have made an important scientific advance by describing the regulatory mechanisms for two members of a new family of ion channels found in non-excitable cells. Their discoveries may pave the way for novel treatments for a variety of conditions, including immune system diseases, blood disorders, liver and kidney failure, strokes, damage from aging, and insulin shock. Their findings are published in two articles in this week's issue of the journal Nature.

Ion channels are tiny molecular pores in cells. These pores control the entry and exit of substances such as sodium, potassium and calcium into the body's cells.

In electrically excitable cells, such as those in the brain and the heart, ion channels help drive the electrical system that runs the body and generate electrical signals between cells.

At one time, scientists thought only nerve cells had ion channels. Later, ion channels were discovered in the pulsating cells of heart muscle. Now, scientists believe virtually every type of cell has ion channels.

Ion channels in the excitable cells of the brain, nerves and cardiovascular system have been extensively studied. These ion channels are the direct or indirect target of about one-third of all current medications. Malfunctions of these ion channels are at the root of epilepsy as well as heart arrhythmia and some other cardiovascular disorders.

In contrast, much less is known about the ion channels in non-excitable cells, such as blood cells, immune system cells, liver and kidney cells, and the cells lining the inside of blood vessels. The latest findings, appearing in this week's Nature articles, represent a significant advance in understanding how non-excitable cells regulate the inflow and outflow of sodium, calcium and related substances. Information on how these new types of ion channels function may lead to improved therapies for diseases of the blood, kidney, liver, arteries and immune system, as well as be
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Contact: Pam Sowers
sowerspl@u.washington.edu
206-685-4232
University of Washington
30-May-2001