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Neurochemical and Cardiovascular Effects of β‐Methylphenethylamine (BMPEA) Analogs Found in Dietary Supplements
Author(s) -
Baumann Michael H.,
Thorndike Eric B.,
Rice Kenner C.,
Schindler Charles W.
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.682.5
Subject(s) - chemistry , neurochemical , amphetamine , dopamine , stimulant , amine gas treating , transporter , pharmacology , dopamine transporter , norepinephrine , norepinephrine transporter , mazindol , medicine , endocrinology , stereochemistry , biochemistry , organic chemistry , gene
Dietary supplements often contain additives not listed on the label. β‐Methylphenethylamine (BMPEA, 2‐phenylpropan‐1‐amine), a structural isomer of the stimulant drug amphetamine, is one such additive. The objective of this study was to determine the neurochemical and cardiovascular effects of BMPEA and its analogs, N ‐methyl‐2‐phenylpropan‐1‐amine (MPPA) and N,N ‐dimethyl‐2‐phenylpropan‐1‐amine (DMPPA). Synaptosomes were prepared from rat caudate tissue for dopamine transporter (DAT) assays or from whole rat brain minus caudate and cerebellum for norepinephrine transporter (NET) assays. Five male Sprague‐Dawley rats received surgically‐implanted telemetry transmitters for the measurement of blood pressure (BP), heart rate (HR) and locomotor activity. Rats were placed into acoustical cubicles for 3 h each weekday, and drug or vehicle was administered on Tuesdays and Fridays. As expected, amphetamine was a potent substrate‐type releasing agent at DAT (EC 50 =5 nM) and NET (EC 50 =8 nM). Like amphetamine, BMPEA was a releaser at DAT (EC 50 =627 nM) and NET (EC 50 =125 nM), and MPPA had similar effects. DMPPA was a weak substrate only at NET (EC 50 =1337 nM). In general, the transmitter releasing actions of BMPEA analogs were more potent at NET than DAT. Amphetamine (0.3–3.0 mg/kg, sc) produced significant dose‐related increases in BP, HR and activity (all F [4,34] > 8.9, p < 0.05). By contrast, BMPEA, MPPA and DMPPA (3.0 and 30 mg/kg, sc) produced significant increases in BP (all F [3,27] > 4.1, p < 0.05) but failed to clearly affect HR or activity. The hypertensive effect of BMPEA was reversed by pretreatment with the α‐adrenergic antagonist prazosin. Our results show that BMPEA and its analogs are biologically active. Although these compounds are unlikely to be abused due to weak effects at DAT, they could produce adverse cardiovascular complications due to prominent transmitter releasing activity at NET. Support or Funding Information Supported by IRP, NIDA, NIH, DHHS. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .