Experimental drug shows promise in reversing high blood pressure's toll on kidneys and heart in mice

High blood pressure, also known as hypertension, affects nearly 1 in 8 people globally and can lead to severe damage to vital organs such as the heart, kidneys, and brain. Two major biological mechanisms contribute to high blood pressure: overactivity of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS), which are the primary targets of most standard blood pressure medications.

A new study published in Communications Biology has focused on a potential driver often overlooked: inflammation. The researchers tested whether Compound17b (Cmpd17b), a drug that targets formylpeptide receptors (FPRs), could repair damage caused by long-term high blood pressure and inflammation to blood vessels and kidneys in mice.

The study found that Cmpd17b lowered average arterial pressure by 6 mmHg in hypertensive mice without affecting those with normal blood pressure. Moreover, the drug reduced kidney scarring and improved aortic flexibility in hypertensive mice, although it did not restore full function to the smaller blood vessels. While these early results are promising, further research in larger animal models and human trials is needed before Cmpd17b could be considered for clinical use.