Elevated blood pressure might stem from the nervous system, potentially caused by overactive neurons. Therefore, dampening neural activity could unveil novel therapeutic avenues.
Researchers affiliated with the University of Missouri and the University of Oxford investigated potential linkages between the excitability of specific neurons within the hypothalamus and the onset of primary hypertension. Their findings were featured in the journal Cardiovascular Research.
High blood pressure is exceedingly common and recognized as a significant risk factor for numerous other health complications, such as strokes and heart attacks, the investigators explain.
Contributing factors can include insufficient physical exercise, poor dietary habits, and ongoing stress; moreover, kidney ailments, hormonal imbalances, and various other elements might also push blood pressure upward. However, the nervous system’s role in this process has remained substantially unclear until now.
While prior investigations already hinted that hypertensive individuals typically exhibit heightened activity in hypothalamic neurons—the brain region governing neuroendocrine functions and the sympathetic nervous system—it was uncertain exactly how this affected blood pressure levels, as noted by the research team.
In the present study, scientists utilized rats to explore the extent to which neurons in the paraventricular nucleus of the hypothalamus, which govern the release of corticotropin hormone, might contribute to hypertension development.
Corticotropin, acting as a hormone, exerts a considerable effect on the operation of both the neuroendocrine and autonomic nervous systems, and is also crucial for stress responses.
“In an animal model exhibiting primary hypertension, we observed an upregulation in the activity of the sympathetic nervous system, which oversees the ‘fight or flight’ response and many involuntary bodily functions,” states study author De-Pei Li from the University of Missouri.
The research cohort examined the degree to which neurons residing in the paraventricular nucleus of the hypothalamus, responsible for managing the ‘fight or flight’ response and numerous autonomous functions, might also foster hypertensive conditions. In hypertensive rats, the team noted not only increased firing of corticotropin-regulating neurons but also crosstalk with neurons in a brainstem area vital for cardiovascular control.
Furthermore, the researchers documented elevated activity in neuroendocrine cells, the components responsible for mediating communication between the neural and endocrine systems.
By suppressing the activity of these specific neuroendocrine cells, the researchers successfully managed to lower blood pressure in the rats, additionally pinpointing a receptor responsible for the communication link between these neuroendocrine cells and the sympathetic nervous system neurons.
“Our data suggest that a compound capable of blocking this receptor could represent a fresh treatment pathway for primary hypertension,” Li added. Further scientific inquiry is required to identify such a therapeutic agent.
Overall, the study’s outcomes strongly indicate that hyperactive neurons in the hypothalamus exert a pronounced influence on blood pressure dynamics and can play a role in initiating and sustaining primary hypertension. Crucially, however, this also illuminates promising directions for future treatment strategies.
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