Scientists in Australia and Singapore have identified inflammatory pathways as a major factor in the development of high blood pressure, presenting a new approach to managing the condition. The findings, published in the journal Communications Biology, suggest that targeting inflammation could play a far more significant role in treating hypertension than previously understood.
The research team demonstrated that an experimental drug known as compound 17b was effective at lowering blood pressure in laboratory mice. The compound also restored damage to blood vessels and organs caused by chronic inflammation.
Chronic inflammation occurs when the immune system becomes excessively active and remains continuously in attack mode. Rather than assisting recovery, this prolonged activation damages tissues over time and is connected to both the sympathetic nervous system and the renin-angiotensin-aldosterone system.
Hypertension is a chronic medical condition in which the force of blood against artery walls remains consistently high. The sympathetic nervous system regulates the body's involuntary fight or flight responses, while the renin-angiotensin-aldosterone system controls fluid balance and blood pressure through hormone regulation.
Targeting inflammation in hypertension
Existing anti-inflammatory treatments generally work by broadly suppressing immune system activity. However, researchers noted that suppressing the immune system too heavily can sometimes increase blood pressure levels rather than lower them.
By contrast, compound 17b operates with greater precision by activating the body's natural mechanisms for resolving inflammation. Instead of shutting down immune responses, the compound prompts the system to prevent overreaction from occurring in the first place.
The experimental drug had previously been shown to protect heart tissue from damage. In mouse trials, researchers directed the drug toward formyl peptide receptors, which act as cellular switches on immune and tissue cells to signal when immune tasks are completed.
Formyl peptide receptors are specialized proteins found on cell surfaces that help coordinate the end of an inflammatory response. Communications Biology is a peer-reviewed scientific journal covering research across the biological sciences.
How compound 17b repairs organs
In mice suffering from hypertension, compound 17b produced a moderate reduction in arterial blood pressure. The drug also reduced stiffness in the main aorta and slowed down the accumulation of scar tissue, known as fibrosis, in the heart and kidneys.
The aorta is the largest blood vessel in the body, carrying oxygenated blood directly from the heart to systemic circulation. Fibrosis occurs when excessive fibrous connective tissue forms inside an organ, which can lead to reduced tissue elasticity and long-term organ damage.
Standard hypertension medications focus primarily on lowering the numbers recorded on a blood pressure monitor to reduce the risk of heart attacks and strokes. Researchers stated that compound 17b directly targets organ damage, potentially broadening treatment applications beyond basic symptom management.
Blood pressure targets and exercise
The findings come as health authorities work to improve blood pressure control. In Ukraine, official plans aim to achieve a population blood pressure control level below 140/90 by 2028.
A blood pressure reading of 140/90 millimetres of mercury represents the standard medical threshold for hypertension, where 140 measures systolic pressure during heart contractions and 90 measures diastolic pressure between beats.
Scientists also highlighted that adding just five minutes of daily physical activity can improve health outcomes for individuals living with elevated blood pressure.
