
Researchers have pinpointed a brain region that might be central to the progression of hypertension. This area is identified as the lateral parabrachial nucleus—a segment in the brainstem responsible for fundamental bodily processes like respiration and heart rate regulation. The findings of this study have been featured in the journal Circulation Research (CR).
According to the lead author, Professor Julian Paton from the University of Auckland, this specific region becomes stimulated during what is termed “forced” exhalation—such as that occurring during bouts of laughter, coughing, or strenuous physical activity.
“In these instances, abdominal muscles are engaged, whereas in regular breathing, exhalation happens passively due to the elasticity of the lungs,” Paton commented.
The investigative team determined that the lateral parabrachial nucleus is interconnected with neural pathways that govern the constriction of blood vessels. This connection has a direct bearing on systemic arterial pressure levels.
“We have uncovered a novel brain locus that provokes an increase in blood pressure. Indeed, in this context, the brain is playing the primary role,” the scientist concluded.
Experimental evidence demonstrated that this zone exhibits hyperactivity in individuals suffering from hypertension. When the researchers managed to inhibit its function, blood pressure levels reverted to normal parameters. The scientists postulate that specific breathing patterns, particularly those involving active contraction of the abdominal muscles, may contribute to elevated blood pressure. This discovery opens avenues for utilizing respiratory characteristics as both a risk indicator and a diagnostic instrument.
However, directly targeting the brain with pharmaceuticals remains challenging, as medications generally affect the entire organ indiscriminately. Nevertheless, the researchers have devised an alternative strategy. It was discovered that the activity of this brain area is modulated by signals originating from the carotid bodies—small structures situated in the neck that continuously monitor blood oxygen levels. Unlike the brain itself, these peripheral structures are amenable to pharmacological intervention.
“Our intention is to employ a medication that suppresses the activity of the carotid bodies, thereby indirectly ‘deactivating’ this specific brain region,” Professor Paton clarified.
The authors suggest that this therapeutic approach could form the foundation for novel hypertension treatments, especially for patients diagnosed with sleep apnea.