The injection of epinephrine (1 mg/kg) into rats caused a significant increase in the distribution ratio (DR) of previously injected 1-aminocyclopentanecarboxylic acid (ACPC) and α-aminoisobutyric acid (AIB) within 2 h. At the same time epinephrine depressed the concentration of AIB in serum. Epinephrine did not alter ACPC concentration or distribution ratio in the diaphragm of partially eviscerated rats with intact livers and kidney. Additional amino acid transport studies were conducted in vitro using ‘intact’ diaphragm preparations from rats and Krebs-Ringer bicarbonate buffer, pH 7.4, at 37°C. AIB uptake into the intact isolated diaphragm was linear during the first 90 min of incubation. Epinephrine (EPI), 183 µ M, caused a 20- to 30-percent decrease in the rate of AIB uptake during this time. EPI concentrations of 1.83 to 91.3 µM had no significant affect on AIB transport during a 60-min incubation period. EPI, 183–787 µ M diminished uptake 30%. EPI, 183 µ M, had a similar effect on AIB transport into diaphragms from adrenalectomized rats. Varying glucose concentrations from 2.2 to 17.8 mM did not significantly alter the inhibitory response elicited by epinephrine. However, the response to epinephrine was abolished by either 0.0 or 36.5 mM glucose. Isoproterenol, 161–403 µ M did not significantly alter AIB transport in this system. On the other hand norepinephrine, 119 to 239 µ M. caused a 20-percent increase of AIB uptake by the isolated diaphragm. Additionally, glucagon (11.5 µ M) caused a 150-percent increase in AIB uptake into diaphragm muscle in vitro. Injecting 1 mg of EPI/kg 60 min before the preparation of the diaphragm caused a 25-percent increase in AIB uptake. AIB concentrations in the buffer medium were not significantly altered by hormone treatments in any of these studies. These results suggest that the increase in AIB uptake caused by injecting EPI may be an indirect action of the catecholamine and that the direct effect of EPI on AIB transport into diaphragm is inhibitory. The results further suggest that the indirect EPI effect in vivo might be caused by glucagon.

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