Brain breathing mechanism linked to persistent high blood pressure

According to Moraes, rather than modulating the central nervous system directly, the therapeutic approach is to pharmacologically manipulate oxygen sensors to reduce the activity of pFL neurons via ATP (adenosine triphosphate) receptors. In addition to being an energy source for cellular activities, ATP functions as a neurotransmitter in the central and peripheral nervous systems (purinergic transmission).

'The silent killer'

Hypertension is the most significant risk factor for cardiovascular disease and is one of the leading causes of heart attacks, strokes, and chronic kidney disease. Several factors influence blood pressure levels, including smoking, alcohol consumption, obesity, stress, high salt intake, high cholesterol, and a lack of physical activity.

In Brazil, data from the Ministry of Health indicates that hypertension affects approximately 30% of adults. Last year, the Brazilian Societies of Cardiology (SBC), Hypertension (SBH), and Nephrology (SBN) issued a new recommendation that changed the blood pressure threshold considered risky, aligning the guidelines with international standards.

The well-known "12 x 8" (systolic blood pressure of 120 mmHg and diastolic blood pressure of 80 mmHg) is now classified as prehypertension, which warrants attention and reinforcement of preventive measures. Normal blood pressure must remain below this threshold.

Research methodology

The scientists used advanced techniques to manipulate and record neuronal activity in rats.

They manipulated the pFL neurons using viral transfection, a technique that introduces genes into cells via modified viruses. This technique does not cause disease; rather, it reprograms specific cells to help scientists understand how the brain controls certain functions, such as blood pressure and breathing.

Optogenetic activation triggered active exhalation and positively modulated sympathetic activity, raising blood pressure. In contrast, pharmacogenetic inhibition eliminated exhalation-related sympathetic excitation and normalized blood pressure in hypertensive rats.

"It had never been demonstrated that neurons that generate expiratory activity communicated with those that control sympathetic activity and blood vessel diameter to impact blood pressure. This was a groundbreaking finding of the study," adds Moraes, who collaborated with researchers from the Ribeirão Preto School of Medicine (FMRP-USP) and the Cardiac Research Center at the University of Auckland's Faculty of Medical Sciences (New Zealand).

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