Thiazides prevent salt from moving through the kidney, causing it to expel salt and water. However, the researchers found that the kidney seems to know “that it’s losing too much salt and activates mechanisms to retain salt in other ways,” said Paul Welling, a professor of physiology at the University of Maryland.
The researchers studied an animal model designed to prevent salt retention, which imitated the thiazides’ effects. They discovered almost 400 genes that alter their activity to assist regulation of the kidney’s salt control. Eventually, it might be possible to make drugs that affect the body’s mechanisms that control how the body interacts with thiazides.
Welling and his colleagues also may have discovered a “biomarker” that could allow doctors to easily find out in which patients thiazides will not work. When the kidney is working against the thiazides, a certain molecule increases in the urine. “Now that we know more about these novel pathways and processes, we can begin to find new ways to help patients with high blood pressure,” said Dean E. Albert Reece, vice president for medical affairs at the University of Maryland.