In a move 14 years ago, inspired by the early 20th century poet Robert Frost, professor of pharmacology Tahir Hussain decided to take an uncommon path in medicine.
Now, with a $1.7 million grant from the National Institutes of Health, Hussain’s lab is studying the ‘less-traveled’ biochemical pathway to prevent kidney damage and salt-sensitive hypertension.
“I decided to take the road less traveled and study an overlooked path, and maybe something will come out of it,” Hussain said.
Hussain’s previous work was studying the role of angiotensin II (AT2) as a protective component of the hormone system responsible for regulating sodium concentration in the blood. After working on this receptor for over a decade, he concluded that AT2 increases sodium excretion and lowers blood pressure, both of which are vital to preserving the kidneys.
Eager to follow this line of research, he decided to continue his work with this hormone, while also choosing to investigate another receptor, Mas, in complement to AT2.
“When I began studying this, not many people were interested in it,” Hussain said. “Now, there are many previous doubters working on this aspect in major labs.”
As of September, Hussain and his research associates Sanket Patel, Elizabeth Gray and Emilio Lucero are investigating whether AT2 and Mas receptors create synergy in working together to protect the kidney.
“The medical community doesn’t know how kidney disease starts,” Hussain said. “We know what causes injury, conditions like diabetes, hypertension and obesity, but there is no drug to treat kidney disease itself.”
Because the kidney’s hormone system isn’t as well studied as other organs like the brain or heart, they hope to find alternative drugs which utilize this combination of receptors to improve the health of patients.
“There are only two types of drugs on the market that protect the kidney from further damage after injury caused by diabetes, hypertension and obesity,” Gray said. “We aim to work with the renin-angiotensin system, which regulates kidney function, to discover some new treatments.”
Lucero said that one-third of diabetic patients die from kidney-related disorders.
The most common of these fatal complications is diabetic nephropathy, when tiny blood vessels are damaged by high concentrations of sugar or salt in the blood, to the point where they can no longer filter properly.
“With the incidence of diabetes on the rise, this research could help in the hypertension prevention effort for decades to come not only in the United States, but all around the world,” Lucero said.
Hussain anticipates working with a chemist to create a bi-functional medication that activates the AT2 and Mas receptors at the same time.
Hussain said that this research dates back to 2003.
“This whole story started in 2003, when my first Pharm.D student brought me astounding results from an AT2 experiment,” Hussain said. “And that has made all the difference.”