Scientists have uncovered a biological pathway that may play a significant role in high blood pressure, opening the door to the development of new treatments that target inflammation and organ damage associated with the condition, in addition to lowering blood pressure itself.
High blood pressure is known to be one of the most prominent risk factors for heart disease and strokes, and is usually associated with several mechanisms within the body, most notably the activity of the sympathetic nervous system and the renin-angiotensin-aldosterone system, which is responsible for regulating blood pressure and the volume of fluids in the body.
But a new study published in the journal Communications Biology suggests that another mechanism, known as "inflammation de-inflammatory pathways," may also play an important role in high blood pressure.
These pathways work to end the inflammatory response when the body no longer needs it, helping the immune system return to its normal state instead of continuing inflammation that could lead to tissue and organ damage.
Researchers from institutions in Australia and Singapore conducted experiments on mice to study the relationship between these pathways and high blood pressure, and tested an experimental compound known as "B17," which activates formalin peptide receptors (FPRs), receptors involved in regulating the immune cell response to inflammation.U
Experiments showed that the compound helped lower blood pressure in mice with hypertension, reduced aortic stiffness, and lessened scar tissue buildup or fibrosis in the heart and kidneys.
Interestingly, these effects appeared even though the decrease in blood pressure was limited, leading researchers to believe that the compound may provide benefits beyond simply lowering blood pressure, by reducing inflammation and helping to repair damaged tissue.
This approach differs from some anti-inflammatory drugs that work by suppressing the immune response, as the "B17" compound focuses on activating the natural mechanisms that help the body endinflammation once it is no longer needed.
The researchers said the findings could help improve understanding of the interaction between the nervous and immune systems in high blood pressure, and may pave the way for treatments that target both inflammatory and neural pathways simultaneously.
They added that activating formalin peptide receptors may represent a promising therapeutic strategy for reducing high blood pressure and fibrosis affecting blood vessels and kidneys.
Despite the encouraging results, the research is still in its early stages, as experiments have so far been limited to animal models, and it is still necessary to conduct studies on humans to confirm the effectiveness and safety of the compound.
This does not mean that the compound "B17" can replace currently used blood pressure medications, but it may become a complementary treatment or an option for some patients in the future, if subsequent studies prove its effectiveness and safety in humans.
The study as a whole indicates that in the future, treating high blood pressure may not be limited to lowering blood pressure numbers, but may also include targeting chronic inflammation and the damage it causes to the heart, kidneys, and blood vessels.
