Tyrosine loading enhances catecholamine excretion by rats.

Tyrosine administration to rats causes dose-related increases in urinary catecholamine levels without reducing tissue catecholamines. Pretreatment with carbidopa, a peripheral inhibitor of aromatic-L-amino acid decarboxylase, reduces basal urinary catecholamine levels and blocks of urinary catecholamine increases caused by tyrosine administration or cold exposure. DOPA excretion, which is usually undetectable by our methods, becomes significant after carbidopa, and rises a further four-fold when rats are also given tyrosine. These observations suggest that tyrosine availability can affect both catecholamine synthesis in and release from the sympathoadrenal apparatus.