Reference

The effects of b-phenylethylamine on tyramine and dopamine metabolism

The effects of b-phenylethylamine on tyramine and dopamine metabolism. McQuade, Paul S.; Wood, Paul L. (Res. Cent., Douglas Hosp., Verdun, PQ, Can.). Prog. Neuro-Psychopharmacol. Biol. Psychiatry, 7(4-6), 755-9 (English) 1983. CODEN: PNPPD7. ISSN: 0278-5846. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) The administration of deuterated b-phenylethylamine (PE) [64-04-0] to mice increased the concns. of deuterated p-hydroxyphenylacetic acid (p-HPAA) [156-38-7] and m-hydroxyphenylacetic acid (m-HPAA) [621-37-4] within the caudate nuclei 2 h after injection. Deuterated m-HPAA concns. remained elevated 4 h after injection of PE. This suggests that high concns. of PE stimulate synthesis of the tyramines and thus of their deaminated metabolites. Deuterated PE rapidly increased the concns. of endogenous nondeuterated p-HPAA and m-HPAA. p-HPAA concns. remained elevated 2 h after PE administration. Thus PE mobilizes the tyramines and elevates concns. of their deaminated products. PE injected into rats initially increased 3-methoxytyramine (3-MT) [554-52-9] concns. in the caudate nuclei. DOPAC [102-32-9] concns. were elevated 5 min later followed by elevated homovanillic acid [306-08-1] concns. Dopamine (DA) [51-61-6] synthesis was also stimulated. The PE-dependent increase in DA release into the synapatic cleft (3-MT increases) and DA synthesis also appears to lead to increased intraneuronal DA metab. (DOPAC increases).

Influence of blind loop on the pharmacokinetics of dopamine and sulfasalazine

Influence of blind loop on the pharmacokinetics of dopamine and sulfasalazine. Thithapandha, Amnuay (Fac.Several substances are used for example 144-83-2 and 102-32-9 which are their cas registry numbers. Sci., Mahidol Univ., Bangkok, Thailand). Pharmacol. Res. Commun., 9(3), 269-77 (English) 1977. CODEN: PLRCAT. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) In order to test the formation of m-hydroxyphenylacetic acid (MHPAA) [621-37-4] from dopamine (I) [51-61-6] and the release of sulfapyridine [144-83-2] from sulfasalazine [599-79-1], self-filling blind loops were created in the jejuna of conventional rats. When dopamine (100 mg) was administered to both control and blind-loop animals, the ratio of MHPAA excreted in the 1st 24 h to that in the 2nd 24 h averaged 12.2 (range 3.8 to 44) in animals with blind loops and 0.09 (range 0 to 0.16) in controls. The presence of a blind loop did not affect the excretion of homovanillic acid [306-08-1] and dihydroxyphenylacetic acid [102-32-9], urinary metabolites of dopamine not derived from bacterial metab. A similar conclusion was also drawn from studies with sulfasalazine (10 mg). A significantly greater quantity of sulfapyridine was excreted in the 1st 6 h in rats with blind loops than in controls. These studies indicate that the presence of a blind loop of the rat's small intestine is assocd. with significant alteration in the kinetics of urinary excretion of flora dependent metabolites of dopamine and sulfasalazine. This observation might serve as the basis for a new method of detecting bacterial overgrowth. .