![MRI scans of human brains.](https://brocku.ca/brock-news/wp-content/uploads/2024/08/GettyImages-1880343100-1600x1067.jpg?x91846)
A Brock research team has shed light on a part of the brain that regulates blood pressure, possibly leading to new medical treatments down the road.
High blood pressure can stem from a number of causes, including the activity of the brain’s sympathetic nervous system, the “fight or flight” response that causes the heart to beat faster and blood vessels to constrict.
Assistant Professor of Kinesiology Stephen Klassen says that with age, the sympathetic nervous system – critical for blood pressure regulation in healthy humans – starts to fail and become overactive, contributing to high blood pressure and cardiovascular diseases.
While much is known about this system, particular components are not well understood.
![: Assistant Professor of Kinesiology Stephen Klassen (left) and his PhD student Nathan Iannarelli (right) stand in front of a wire trolly with a computer screen in the middle displaying colourful images, with a blurry research poster in the background.](https://brocku.ca/brock-news/wp-content/uploads/2024/08/SteveAndNathan01-1050x700.jpg?x91846)
Assistant Professor of Kinesiology Stephen Klassen (left) and his PhD student Nathan Iannarelli found that a specialized type of receptor in the brain is important for regulating the strategies the sympathetic nervous system uses to control blood pressure.
In a recently published paper, Klassen and PhD student Nathan Iannarelli examined how the sympathetic nervous system communicates with the blood vessels to regulate blood pressure.
To do so, the sympathetic nervous system sends out electrical impulses along nerves, which release chemicals called neurotransmitters that change the activity of the heart and blood vessels.
Many mechanisms in the brain can alter the activity of the sympathetic nervous system including neurons with a specialized type of receptor called alpha-2 adrenergic receptors.
Receptors are responsible for communicating between neurons and other organs.
“How alpha-2 adrenergic receptors regulate the electrical impulses travelling along sympathetic nerves controlling the blood vessels is not well understood,” says Klassen.
In collaboration with investigators at Mayo Clinic in Minnesota and the University of Western Ontario, he and Iannarelli recruited eight healthy people for the study.
Participants were given a medication called dexmedetomidine, which binds to and activates alpha-2 adrenergic receptors in the central nervous system. This enabled the researchers to get a close look at how these receptors work.
“We found that alpha-2 adrenergic mechanisms in the brain are important for regulating the strategies the sympathetic nervous system uses to control blood pressure including the firing of differently sized sympathetic nerves and the speed of the neural impulses travelling along the nerves,” says Iannarelli. “This research is important for advancing our knowledge regarding the mechanisms that regulate the sympathetic nervous system for blood pressure regulation in humans.”
Iannarelli says future research can build on the team’s findings to explore the potential involvement of alpha-2 adrenergic mechanisms in age- and disease-related failures in the sympathetic nervous system.
Additional studies may also boost the use of current drugs like clonidine or development of new medications that selectively target alpha-2 adrenergic receptors for lowering sympathetic neural activity and blood pressure, he says.
Supporting the team’s research were grants from the Natural Sciences and Engineering Research Council of Canada, which is funded by the Government of Canada, the Ontario Graduate Scholarship Program, the American Heart Association and the U.S. National Institutes of Health.
The duo’s findings can be found in their study, “Central µ2-adrenergic mechanisms regulate human sympathetic neuronal discharge strategies,” published in July in The Journal of Physiology.