Taking Histamine To Heart (And Kidneys)

Despite its association with allergy and inflammation, histamine protects against heart and kidney damage in cardiorenal syndrome.

AsianScientist (Feb. 24, 2020) – A team of scientists in Japan has found that histamine, associated with allergies and inflammation, could alleviate heart and kidney damage in cardiorenal syndrome. Their findings are published in the Proceedings of the National Academy of Sciences.

Chronic kidney disease and heart failure are critical medical problems worldwide and are closely associated in a phenomenon known as cardiorenal syndrome. Many studies have attempted to understand the complex relationship between kidney and heart dysfunction, but few have provided a clear target for treatment.

In the present study, researchers led by Professor Akiyoshi Fukamizu at the University of Tsukuba, Japan, found that mice with cardiorenal damage had higher levels of histamine in their blood than normal mice.

“Histamine is an important factor in various inflammatory processes, and its inhibition generally leads to better disease control,” said Fukamizu. “We found elevated levels of histamine in a mouse model of cardiorenal syndrome, which, surprisingly, protected the mice against further organ damage.”

Mice that could not produce histamine showed worse cardiorenal damage effects, including increased heart size, altered cardiac contractility and poor urinary filtration. Similar effects were observed when a specific histamine receptor (H3) antagonist was administered to mice with cardiorenal damage. On the other hand, stimulating the H3 receptor markedly alleviated the symptoms of cardiorenal syndrome.

These findings suggest that the H3 receptor is a druggable target that could be used to prevent damage to the heart and kidneys in cardiorenal syndrome, although further studies are needed to confirm if these findings can be replicated in humans.

The article can be found at: Noguchi et al. (2020) Histamine Receptor Agonist Alleviates Severe Cardiorenal Damages by Eliciting Anti-inflammatory Programming.


Source: University of Tsukuba; Photo: Shutterstock.
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