Effects of imipramine on tyrosine and tryptophan are mediated by β-adrenoceptor stimulation

doi:10.1016/0024-3205(88)90659-5

Life Sciences

Volume 42, Issue 7, 1988, Pages 853-862

https://doi.org/10.1016/0024-3205(88)90659-5 Get rights and content

Abstract

Imipramine (IMI; 20 mg/kg) in rats decreased the plasma tyrosine concentration by 21% (90 min), whereas norepinephrine (NE; 1.25 mg/kg) raised it by 72% (40 min). Since NE raised plasma tyrosine by stimulating α-adrenoceptors, as shown by phenoxybenzamine (PB) completely abolishing this increase, an experiment was done to find out whether IMI lowered plasma tyrosine by blocking α-adrenoceptors. In contrast to PB, IMI pretreatment failed to alter the NE-induced elevation in plasma tyrosine, suggesting that at this dose IMI is not an effective α-adrenergic antagonist $in vivo$ . Thus, IMI would not appear to reduce plasma tyrosine by blocking α-adrenoceptors. In a separate experiment, propranolol blocked the ability of IMI to lower plasma tyrosine. Propranolol also prevented a 17% elevation in brain trytophan levels induced by IMI but did not alter the 29% decrease in plasma tryptophan. OB by itself decreased plasma tyrosine, but this decrease was not greater by additionally treating with IMI. Salbutamol (10 mg/kg), a β₂ agonist, lowered plasma tyrosine to 76% and raised brain tryptophan to 143% of control. These results suggest that IMI decreases tyrosine concentrations in plasma and raises tryptophan in brain by stimulating β-adrenoceptors.

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Effects of imipramine on tyrosine and tryptophan are mediated by β-adrenoceptor stimulation

Abstract

Pharmacol. Ther.

Biochem. Pharmacol.

Life Sci.

J. Chromatogr. Biomed. Applic.

Biol. Psychiat.

Life Sci.

Neuropharmacology

Life Sci.

J. Biol. Chem.

Eur. J. Pharmacol.

Life Sci.

Rev. Physiol. Biochem. Pharmacol.

J. Pharmacol. Exp. Ther.

Psychopharmacology

Science

Naunyn-Schmiedeberg's Arch. Pharmacol.