l-amphetamine affects on SNS (Journal references)
I looked through extensive journal databases in hopes to find much on the affects of l-amphetamine on the SNS. I found one article.
I also found this.
I understand that rats/dogs and humans are different indeed but this is stating that the l-isomer is 4x less potent than the d-isomer in inhibiting MAO-A and 5x less potent in increasing blood pressure? l-isomer also appears to be 3x less potent in producing tachycardia.
Does anyone have any other document links that show evidence for pressor or cardiac responces due to the alpha-methyl PEA isomers. To me the above articles state the opposite of what is thrown around about the isomers.
Maybe l-meth is different than l-amph?
MAO-A inhibition is generally known to increase blood pressure and heart rate in the presence of stimulants which some may know by experience.
I looked through extensive journal databases in hopes to find much on the affects of l-amphetamine on the SNS. I found one article.
Both d- and l-amphetamine were also compared for their pressor and tachycardic activity in pithed rats. The doses of amphetamine tested (0.1-10.0 mg/kg) were identical to those which produced changes in behavior. d-Amphetamine was approximately 5-fold more potent than l-amphetamine in evoking pressor responses and approximately 3-fold more potent in evoking tachycardic responses.
http://jpet.aspetjournals.org/cgi/content/abstract/193/1/149
I also found this.
In vitro inhibition of monoamine oxidase types A and B by d- and l-amphetamine
Miller, H.H., Clarke, D.E., (1978) Communications in Psychopharmacology 2 (4), pp. 319-326
Dept. Pharmacol., Coll. Pharm., Univ. Houston, Tex. 77004, United States
Abstract:
Experiments were made in vitro to investigate the monoamine oxidase (MAO) inhibitory properties of d- and l-amphetamine. The MAO inhibitory potency of d-amphetamine was found to be greatest in tissues showing high type A activity (heart > striatum = vas deferens > liver). Comparisons of d- and l-amphetamine on only the type B activity revealed that the enantiomers were essentially equipotent, yielding an IC50 of approximately 1.1 x 10-3 M. Both enantiomers were more potent at inhibiting type A MAO, with an approximate IC50 of 1.2 x 10-4 M for l-amphetamine and 2.8 x 10-5 M for the d-form. Thus, on type A MAO, d-amphetamine is over four fold more potent than l-amphetamine. These potency ratios remained closely similar regardless of the tissue studied. The data suggest that inhibition of type A MAO by d-amphetamine may be an important pharmacologic property of the drug in vivo. Furthermore, the individual characteristics of the A and B activities do not appear to differ radically across the various tissues studied.
I understand that rats/dogs and humans are different indeed but this is stating that the l-isomer is 4x less potent than the d-isomer in inhibiting MAO-A and 5x less potent in increasing blood pressure? l-isomer also appears to be 3x less potent in producing tachycardia.
Does anyone have any other document links that show evidence for pressor or cardiac responces due to the alpha-methyl PEA isomers. To me the above articles state the opposite of what is thrown around about the isomers.
Maybe l-meth is different than l-amph?
MAO-A inhibition is generally known to increase blood pressure and heart rate in the presence of stimulants which some may know by experience.
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