Dr. Huang said that not everyone who eats too much salt ends up with hypertension, but some population groups, such as African-Americans, are more prone to develop salt-sensitive high blood pressure, suggesting that genetic factors may play a role in the disease.
One extension of the current work may lead to a better understanding of hypertension that is induced by low potassium intake. Previous studies have shown that diuretics, a class of drugs commonly used to control hypertension, also cause potassium wasting, or low potassium levels, in patients.
"Studies have shown that if you are taking diuretics and let your potassium level fall, the diuretics are not as effective," Dr. Huang said. "But if you take diuretics and you supplement with potassium, you can lower blood pressure more effectively." Dr. Huang and his research group currently are conducting studies to determine whether low potassium intake increases WNK1 activity, leading to hypertension.
The WNK1 enzyme was first identified and cloned in 2000 by UT Southwestern researchers led by Dr. Melanie Cobb, co-senior author on the PNAS paper and dean of UT Southwestern Graduate School of Biomedical Sciences. After cloning the enzyme, Dr. Cobb's research group examined what proteins might be regulated by WNK1, and found that SGK1 was one of those proteins. Because he works on ion channels, including sodium channels, Dr. Huang joined efforts with Dr. Cobb to study how WNK1 regulates sodium channels.
"We have been working on WNK1 for several years now and these findings are unexpected from initial studies," said Dr. Cobb. "What is particularly satisfying and exciting is the ease with which we could establish such a collaboration at UT Southwestern to study the physiological and
Source:UT Southwestern Medical Center