Browse evidence-based analysis of health-related claims and assertions
When mice ate a normal diet, growing more lymphatic vessels in their kidneys didn't change how they handled salt or water.
Mice with extra kidney lymphatic vessels had less of two key proteins that reabsorb salt in the kidneys, helping them excrete more salt.
Mice with extra kidney lymphatic vessels on a high-salt diet had more of a hormone that helps the body get rid of salt and water.
Mice with extra kidney lymphatic vessels on a hypertension-inducing drug excreted more sodium relative to their kidney function compared to normal mice.
Growing more lymphatic vessels in mouse kidneys during high-salt intake doubled the amount of fluid in the kidney tissue, acting like a sponge to hold extra fluid.
Mice with extra kidney lymphatic vessels on a high-salt diet excreted 64% more sodium in their urine compared to normal mice, helping them manage salt better.
When mice ate a high-salt diet, growing more lymphatic vessels in their kidneys lowered their blood sodium levels by about 4% compared to mice without extra lymphatic vessels.
Because this model includes detailed blood vessel and kidney cell features, it can simulate diseases and test drug effects.
Older kidney models only worked for one specific condition, but this new model works for many different situations and matches real rat data.
This kidney model is more detailed than other computer models of the whole body or kidney parts.
This is the first computer model to connect blood vessel and kidney tube functions in a single system.
A computer model of kidney function that includes how hormones affect kidney tubes and blood vessels can accurately simulate how the kidneys control salt and water levels in the body.
Mice missing the KDM6A gene in their kidneys show signs of faster aging, like higher levels of certain proteins linked to aging.
Giving Klotho to mice with high blood pressure caused by missing the KDM6A gene in kidneys lowers their blood pressure back to normal.
Mice missing the KDM6A gene in their kidneys show more water-absorbing proteins, which might make them hold onto more water.
When mice lose the KDM6A gene in their kidneys, certain salt-handling proteins increase, which makes it harder for their kidneys to get rid of salt.
When mice lose the KDM6A gene in their kidney cells, their kidneys hold onto more salt and their blood pressure goes up, which might be linked to changes in a specific protein mark.
In mice, AMPK is linked to how the kidneys function.
When mice lose both AMPKα1 and AMPKα2 in their kidneys, they lose too much water and salt in their urine.
Even though these mice have less red blood cells, their blood plasma volume is higher than normal mice.
Mice missing the AMPKα1 gene produce more aldosterone in their urine and have lower blood pressure than normal mice.
When mice lack the AMPKα1 gene, their kidneys handle salt normally and produce less urine than usual.
Kidneys regulate blood volume by controlling sodium and water excretion.
Blood pressure is determined by cardiac output, blood volume, and vascular resistance; an increase in any of these factors elevates blood pressure.