The study will appear in an upcoming issue of the Proceedings of the National Academy of Sciences.
"This is a classic example of how basic research could lead to better understanding of human diseases and potentially to new therapeutic methods," said Dr. Bing-E Xu, assistant professor of pharmacology at UT Southwestern and lead author of the study.
The enzyme WNK1 is known to cause a form of hypertension, abbreviated PHA II, but until now the method by which it affected blood pressure was unclear. By studying animal and human cells in culture, UT Southwestern researchers determined that WNK1 interacts with and activates another enzyme, SGK1, which is well known to lead to the activation of sodium ion channels in kidney cells.
"The kidney plays a very important role in controlling blood pressure by controlling how much sodium gets reabsorbed back into the kidney and the blood," said Dr. Chou-Long Huang, associate professor of internal medicine at UT Southwestern and co-senior author of the study. "Sodium comes into the kidney cell through these channels and is then returned to blood circulation through another sodium transporter," he said. "The sodium channel critically governs how much sodium gets reabsorbed."
Normally, the kidney filters and reabsorbs about 99 percent of sodium from the blood and returns it to the body, excreting 1 percent through urine, said Dr. Huang, a nephrologist.
However, if salt ingestion remains the same a
Source:UT Southwestern Medical Center