High blood pressure and its consequences are the principal cause of death in the industrialized world. Among the numerous medications used to treat the condition, there is a drug called nifedipine. It lowers blood pressure by blocking the calcium channels in the blood vessel walls. But this is not its only effect, as Carolin Zwadlo discovered while preparing her PhD thesis under the supervision of Professor Dr. Jürgen Borlak at the Fraunhofer Institute for Toxicology and Experimental Medicine ITEM in Hanover: “It used to be assumed that the drug acted solely by way of changes to the blood vessels. The textbook view was that the heart was not a direct target for its action,” Zwadlo relates. “But as my research shows, this is only true for a healthy heart. In animals with high blood pressure, nifedipine modifies the genetic code used to make transport proteins.” The function of transport proteins is to enable various types of ion to enter the cells. This allows the cell to maintain its natural equilibrium and permits cell contraction. These modifications to the heart are not necessarily beneficial to the patient. Zwadlo compared the patterns of activated and deactivated genes in animal hearts that had been modified by nifedipine with the patterns found in diseased human hearts. “There was a surprising concordance, which leads to the supposition that nifedipine is capable of producing undesirable effects on the heart. For the safety of patients, it would be appropriate to question the advisability of long-term treatment with this pharmaceutical agent.” Another important finding of Zwadlo’s thesis work is the confirmation that nifedipine does not lead to any changes in a healthy heart – unlike its effect on a diseased heart. “Drug safety tests are usually carried out on healthy animals. Consequently, the results are not always transferable” says Zwadlo. She was awarded the first-place Hugo Geiger Prize, valued at 3000 euros, for her doctoral thesis. In Zwadlo’s opinion, the differing effects of nifedipine on healthy and diseased hearts could possibly be the cause of the adverse effects of prolonged treatment with this drug. So far, however, researchers have not found anything that might explain why these changes should only occur in diseased hearts and not in healthy hearts.
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