The formation and release of metaraminol during exposure to warm or cold environments

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Abstract
Rats were injected intraperitoneally with alpha‐methyl‐m‐tyrosine (400 mg/kg) and placed at either 27° C or 4° C. The levels of alpha‐methyl‐m‐tyramine, metaraminol and noradrenaline were determined in heart tissue after 1, 4 and 12 hr of treatment. The excretion of metaraminol, alpha‐methyl‐m‐tyramine, noradrenaline, adrenaline and 3‐methoxy‐4‐hydroxyphenylglycol (MHPG) was also estimated in both treated and control rats. Cold exposure increased both the formation and excretion of metaraminol. Hearts removed from the cold‐stressed rats 4 hr after injection contained significantly more metaraminol than hearts taken from animals maintained in the warm environment. Twelve hours after treatment, no metaraminol remained in the hearts of cold‐exposed rats, whereas significant quantities of the amine still remained in the hearts of rats kept at 27° C. These results support the false transmitter concept advanced for metaraminol as they demonstrate that in vivo sympathetic stimulation can increase both the formation and release of metaraminol. Alpha‐methyl‐m‐tyrosine produced a greater fall in cardiac noradrenaline in the rats kept at 27° C. Whereas an approximate mole‐for‐mole replacement of metaraminol for noradrenaline existed at 27° C, no such relationships existed at 4° C. Twelve hours after treatment the hearts of cold‐stressed rats contained no metaraminol and only 40% of control noradrenaline levels. These results do not support the necessity for a mole‐for‐mole replacement of noradrenaline with metaraminol to produce a catecholamine loss. Alpha‐methyl‐m‐tyrosine depressed the noradrenaline excretion for at least 24 hr in the cold‐stressed rats. Excretion of 3‐methoxy‐4‐hydroxyphenylglycol was also lower in the treated rats between 0 and 12 hr in the cold but rose abruptly between 12 and 24 hr to exceed the quantity excreted by the control animals. This increase suggests an increase in noradrenaline synthesis, which may be related to the depletion of metaraminol from the body. The results of this paper support the postulate that metaraminol may function as a false transmitter. They do not agree with the concept that the loss of noradrenaline from tissue sites is dependent upon a mole‐for‐mole replacement with metaraminol.