Salt is not all bad, but too much of it can have a serious impact on your cardiovascular health. Reducing our salt intake can seem challenging, however, and new research maps the neurons that make passing up salt so difficult.
A moderate amount of salt is crucial to our health. The sodium found in salt helps the body to contract and relax its muscles, send electric impulses between nerves, and keep fluids at a balanced level.
Additionally, through a delicate interplay between the kidneys, our water levels, and cellular function, sodium helps to regulate blood pressure.
But too much salt can have adverse effects on our health. When there is too much sodium in the blood, and the kidneys cannot cope, the water is sucked out from the cells and moved into the bloodstream.
This increases the volume of blood, making the heart and blood vessels have to work harder in order to keep a healthy blood pressure. Over time, this may stiffen the arteries and increase the likelihood of having a heart attack or stroke.
For these reasons, the Dietary Guidelines for Americans
A team of researchers from the Division of Endocrinology, Diabetes, and Metabolism at the Beth Israel Deaconess Medical Center in Boston, MA, set out to map the brain circuit that underpins our craving for salt.
The scientists were led by Dr. Bradford Lowell, and Jon M. Resch – a postdoctoral researcher in Dr. Lowell’s laboratory – is one of the study’s first authors. Their findings were published in the journal Neuron.
It is a known fact that a sodium deficiency increases two hormones: angiotensin II and aldosterone. Recent studies, the authors explain, have shown that neurons that respond to the angiotensin II hormone, as well as those that respond to aldosterone, drive our appetite for salt.
For the current study, the researchers decided to focus on aldosterone-responsive neurons, which are called NTSHSD2 neurons.
Previous research led by Dr. Joel Geerling – who is also a co-author on the new study – showed that aldosterone-responsive NTSHSD2 neurons are activated by sodium deficiency, but the cellular mechanism through which this happens was unknown.
This is why, in the new study, Resch and colleagues decided to investigate “the cellular and molecular mechanism by which NTSHSD2 neurons are activated by [sodium] deficiency.”
Resch and team activated NTSHSD2 neurons artificially in mice without a sodium deficiency in an attempt to see whether they would experience the same sudden onset of sodium appetite previously observed in sodium-deficient mice.
The researchers found that NTSHSD2 neurons are not enough to drive sodium appetite on their own. It is only in conjunction with signaling from the angiotensin II hormone that mice displayed cravings for sodium.
This led the researchers to believe that there is another subset of neurons that are responsive to angiotensin II, which may have a crucial role in triggering sodium appetite.
These precise neurons are unknown, but the team believes that neurons in the subfornical organ that express the angiotensin II type 1a receptor are “likely candidates.”
“We identified a specific circuit in the brain that detects sodium deficiency and drives an appetite specific for sodium to correct the deficiency,” says Resch.
“In addition, this work establishes that sodium ingestion is tightly regulated by the brain, and dysfunction in these neurons could lead to over- or under-consumption of sodium, which could lead to stress on the cardiovascular system over time.”
Jon M. Resch
“Several questions remain with regard to how sodium appetite works, but a major one is where [angiotensin II] is acting in the brain and how the signal works in concert with NTSHSD2 neurons that respond to aldosterone,” adds Resch.
“We have already begun work to help us close these gaps in our knowledge,” he concludes.