Mysterious role of renin in hypertension unlocked

Last Updated: Monday, October 31, 2011 - 19:30

Sydney: A Sydney medical scientist has finally uncovered a secret central to the cause of high blood pressure after a 40-year long hunt.

Professor Brian Morris and his Sydney University team have found hitherto mysterious role of the enzyme renin in triggering the condition.

The research is the first of its kind to use human kidneys. It opens the way for more targeted drugs, which could transform treatment of high blood pressure, a very strong risk factor for heart attack and stroke.

Morris, one of Australia’s leading genetic scientists, first began studying renin as a young student in the early 1970s.

Now another young scientist, his PhD student, Brazilian Francine Marques, has performed the laboratory work, under his supervision, which helped clinch these new findings that may have international significance.

While renin was thought to play a significant role in high blood pressure, how it worked to achieve this was something that had eluded researchers for many years, Professor Morris noted.

His team identified the decisive role of two micro-RNAs - novel genetic material that has a destabilising effect on the production of renin from its gene.

Their research showed that in hypertensive kidneys the renin gene was six times more active while the micro-RNAs were six times less so.

``”That is the key. These two micro-RNAs are very much lower in hypertensive people. So if you lose those, the renin goes up, thus raising blood pressure,” the Sydney Morning Herald quoted Morris as saying.

“This is a totally new concept … tremendously exciting. No one has ever found anything like this to do with rennin,” he added.

The discovery of the role of the two micro-RNAs could lead to the development of hypertension drugs, which could be designed to “knock down renin expression at its source.”

The study has been published in the online version of Hypertension, the journal of the American Heart Association.

ANI



First Published: Monday, October 31, 2011 - 19:30

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