NONMAST-CELL HISTAMINE KINETICS. III. UPTAKE, METABOlism AND DECLINE OF H³-HISTAMINE IN THE FEMALE RAT AND EFFECTS OF ENDOGENOUS HISTAMINE RELEASE

¹ Life Sciences Research, Stanford Research Institute, Menlo Park, California

Kinetic aspects of distribution and metabolism of injected H³-histamine were studied. The decline of exogenous labeled histamine is biphasic in several tissues of the female rat while approximating a single exponential function in the pyloric stomach. The initial phase of decline, representing primarily catabolism and tissue uptake of circulating histamine, exhibits a duration of 30 to 60 minutes. Over the subsequent two-hour period the decline of both labeled histamine and total labeled metabolites is approximately logarithmic in both fed and fasted rats. In the latter, uptake of H³-histamine was increased in some tissues, and decline of labeled amine was accelerated in pyloric stomach. Tissue uptake of circulating H³-histamine was markedly reduced in anaphylaxis. The isotopic amine, however, was neither released from prelabeled tissue pools by anaphylactic mast-cell histamine release nor was its retention generally enhanced by such treatment. Conversely, nonmast-cell histamine release by reserpine pretreatment did not markedly affect catabolism and tissue uptake of circulating H³-histamine but altered the kinetics of subsequent decline of labeled amine in some tissues. The results indicate that exogenous histamine is taken up from the circulation into kinetically distinct tissue pools. The decline of H³-histamine in such pools appears to be related to in vitro histidine decarboxylase activity and may reflect the turnover of nonmast-cell histamine in several tissues.