Histamine is known to exert profound effects on the cardiovascular system in many mammals. Carnosine (beta-alanyl-L-histidine) is a dipeptide previously known to be present only in a few tissues. It is our hypothesis that carnosine serves as a non-mast cell reservoir for histidine, available for histamine synthesis during periods of physiologic stress. To validate this hypothesis, we demonstrated the existence of carnosine in multiple histamine-rich tissues in several mammalian species; documented a metabolic link between carnosine and histidine, histamine and 3-methylhistamine (a degradation product of histamine) in unstressed animals, and showed that tissue carnosine is decreased simultaneously with an increase in tissue histamine during stress.
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