"We have known for decades that when a particular receptor in the brain is over-stimulated, blood vessels constrict and blood pressure rises," said George Prell, PhD, Associate Professor of Pharmacology and Biological Chemistry at Mount Sinai School of Medicine and first author on the study. "What we didn't know was which molecule in the body was binding to this receptor to trigger this reaction. Now that we have identified this substance, we can begin to look at ways of blocking its action. We also found that excessive accumulation of this molecule in the pancreas will impair insulin release, thus it is possible that this molecule is the long searched for link between these two disorders."
The researchers found that imidazole-4-acetic acid-ribotide binds to imidazol(in)e receptors which are widespread throughout the brain, and are abundant in the brainstem in areas critical to blood pressure regulation. In addition, they found that when this molecule binds to the receptor it leads to elevated blood pressure. When an antagonist (another molecule that blocks the action of the first) is given, imidazole-4-acetic acid-ribotide's high blood pressure effect is inhibited.
While some causes of high blood pressure are clearly established, the majority of cases are considered "essential hypertension," that is high blood pressure for which the cause is unknown. The researchers hypothesize that elevated levels of this ribotide may account for a major fraction of cases of essential hypertension.
In addition, imida
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