The findings are published in today's issue of Nature.
"This calcium transporter really is an important key to understanding how the heart is regulated," said Dr. Donald Hilgemann, professor of physiology and senior author of the study. "At every beat, calcium in heart cells increases. And it's calcium that is the messenger to the heart to get it to contract.
"We knew for a long time that NCX1 brings calcium into and out of heart cells by exchanging it for sodium. And in doing so it generates important electrical currents in the heart. The surprise is that this transporter dances more than just that old waltz from Vienna. It knows Salsa!"
The research reveals two new modes of operation of NCX1. First, the membrane protein can move sodium into heart cells without moving calcium out. This mode generates an electrical current independent of calcium transport that contributes to excitation of the heart. The second mode is to move calcium into heart cells without generating any electrical current. This mode, Dr. Hilgemann said, may determine the calcium that remains in heart cells after each beat and thereby determines the strength of cardiac contraction over many beats.
Using so-called "giant membrane patch" techniques together with highly sensitive ion detection techniques, both developed and implemented by Dr. Hilgemann, UT Southwestern researchers were able to determine precisely how NCX1 works as an ion exchanger, how many calcium and sodium ions move across the membrane, when they are exchanged, and, surprisingly, when they move together.
"Transporters move ions across membranes by grabbing hold of them and transferring the energy of one type of ion to another type, just one
Contact: Amy Shields
UT Southwestern Medical Center