The same brain cells that sense low salt also have a built-in alarm for angiotensin, a hormone that signals low blood volume—so they respond to both signals together.
Scientific Claim
NTSHSD2 neurons express high levels of the angiotensin II receptor AT1aR, and angiotensin II directly increases their firing rate, suggesting they integrate both aldosterone and angiotensin signals to coordinate sodium appetite.
Original Statement
“NTSHSD2 neurons express abundant AT1aR mRNA... bath application of ATII markedly increased the firing rate of NTSHSD2 neurons, and the AT1aR-selective blocker, losartan, blocked this effect.”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
definitive
Can make definitive causal claims
Assessment Explanation
The study directly demonstrates AT1aR expression via RNA-Seq and functional responsiveness via electrophysiology with pharmacological blockade, establishing a definitive mechanistic link within the mouse model.
Evidence from Studies
Supporting (1)
The study shows that certain brain cells that sense low salt also respond to a hormone called angiotensin II, and when both signals are present, they make animals really crave salt—like a team-up between two warning systems.