Dr. Wolfgang Linke of the Ruhr-Universitat Bochum Institute of Physiology, in cooperation with colleagues from the Mayo Clinic in Rochester, Minn., said the drug activates an enzyme that causes the giant protein titin in the myocardial cells to relax.
"We have developed a therapy in an animal model that, for the first time, also raises hopes for the successful treatment of patients," Linke said in a statement.
Sildenafil inhibits a specific enzyme (phosphodiesterase 5 A), which causes the increased formation of a messenger substance (cGMP). The messenger substance activates the enzyme protein kinase G, which attaches phosphate groups to certain proteins.
The researchers found the cardiac muscle protein titin is also phosphorylated through the same mechanism.
"The titin molecules are similar to rubber bands," Linke said. "They contribute decisively to the stiffness of the cardiac walls."
The activity of the protein kinase G causes titin to relax, making the cardiac walls more elastic, within minutes of administering the drug.
"If, for the first time, the drug is found to have a positive effect on heart failure, we would already have a molecular mechanism on hand to explain the effect," Linke said.
The findings are published in the journal Circulation.