New rodent research reveals surprising insights into the relationship between neuron activity and blood flow, as well as how salt consumption affects brain.
Basically, to use the words of Javier Stern, author of the study, "When you ingest salty food the brain senses it and activates a series of compensatory mechanisms to bring sodium levels down."
What does it mean?
When neurons are activated, there is usually a rapid increase in blood flow to the area. This relationship is known as neurovascular coupling or functional hyperemia and occurs by dilating blood vessels in the brain called arterioles. Previous studies of neurovascular coupling have been limited to superficial areas of the brain (such as the cerebral cortex). Scientists studied how blood flow changes in response to the environment (such as visual or auditory stimuli). Little is known whether the same principles apply to deeper brain regions in tune with the stimuli produced by the body itself, known as interoceptive signals.
The brain ... in salt
To study this relationship between salt and the brain in its deep regions, a team of scientists led by Javier Stern, a neuroscience professor at Georgia State University, has developed a new approach. This approach combines surgical techniques and advanced diagnostics. The team focused on the hypothalamus, a deep brain region involved in critical body functions including drinking, eating or regulating body temperature, and also involved in reproduction. The study, which appears in Cell Reports magazine, examines how blood flow to the hypothalamus has changed in response to salt intake.
“We chose salt because the body needs to control sodium levels very precisely. We also have specific cells that detect the amount of salt in the blood, "Stern says.
When you ingest salty food, the brain senses it and activates a series of compensatory mechanisms to bring sodium levels down. The body does this in part by activating the neurons that trigger the release of vasopressin, an antidiuretic hormone that plays a key role in maintaining the correct salt concentration.
What changes? Surprise results.
In contrast to previous studies that observed a positive link between neuron activity and increased blood flow, the researchers found a decreased blood flow when neurons are activated in the hypothalamus.
"The results took us by surprise because we saw vasoconstriction, which is the opposite of what most people have described in the cortex in response to a sensory stimulus," says Stern. "Normally there is a reduction in blood flow in the cortex in the case of diseases such as Alzheimer's or after a stroke or ischemia."
The team calls the phenomenon "reverse neurovascular coupling" or a decrease in blood flow that produces hypoxia. They also observed other differences: in the cortex, the vascular responses to stimuli are very localized and dilation occurs rapidly. In the hypothalamus, the response was widespread and occurred slowly, over a long period of time.
"When we eat a lot of salt, our sodium levels stay high for a long time," says Stern. "We believe hypoxia is a mechanism that strengthens the ability of neurons to respond to prolonged salt stimulation, allowing them to remain active for an extended period."
Salt, hypertension and hypoxia
The findings raise interesting questions about how hypertension can affect the brain. It is believed that between 50 and 60% of hypertension is due to salt, i.e. it is triggered by excessive salt intake. The research team intends to study this reverse neurovascular coupling mechanism in animal models to determine whether it contributes to the pathology of hypertension. Additionally, they hope to use their approach to study other brain regions and diseases, including depression, obesity, and neurodegenerative conditions.
“If you chronically ingest a lot of salt, you will have an overactivation of the vasopressin neurons. This mechanism can then induce excessive hypoxia, which could lead to tissue damage in the brain, "says Stern." If we can better understand this process, we can devise new targets to stop this hypoxia-dependent activation and perhaps improve the results of people with salt-dependent arterial hypertension ".
