Hypertension helped by immune cells, says study
High blood pressure or hypertension is a leading cause of life-threatening conditions including heart attack, kidney disease and stroke.
A study of cells in the immune system could be the answer to tackling instances of high blood pressure, as observed by researchers from the University of Edinburgh.
The study, which was funded by the British Heart Foundation and published in the European Heart Journal, revealed that specialised white blood cells – known as macrophages, central to the body’s immune system – scavenge for and ‘eat’ molecules of a powerful hormone named endothelin. The endothelin is responsible for raising blood pressure through blood vessel constriction.
The results of the study also showed that lowering levels of macrophages increased blood pressure in mice fed a high salt diet. When the macrophage level returned to normal, blood pressure also normalised in the mice.
The discovery could help identify people most at risk of developing hypertension, spotlighting current treatments that could increase risk of the disorder, which affects more than 12 million people in the UK, and thus opening avenues to improve these treatments, although caution that further human studies are needed have been raised.
Professor Matthew Bailey of the university’s British Heart Foundation Centre of Research Excellence and a chair of renal physiology at the university, who led the study, has said that it exposes risk factors and allows for the investigation of new drugs that could help patients. They will further examine the role of macrophages in hypertensive patients, as hypertension affects millions of people across the globe – some 70% of people over 70.
It is therefore important to make necessary lifestyle choices tomitigate a hypertension diagnosis: eat healthily and maintain good weight through regular exercise, limit alcohol and salt consumption, and most importantly, monitor your blood pressure.
Subscribe
If you enjoyed this article, subscribe to receive more just like it.
