RT Journal Article
SR Electronic
T1 ON THE MECHANISM OF HEART NOREPINEPHRINE DEPLETION BY TYRAMINE, GUANETHIDINE AND RESERPINE
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 399
OP 404
VO 144
IS 3
A1 Ronald Kuntzman
A1 Martin M. Jacobson
YR 1964
UL http://jpet.aspetjournals.org/content/144/3/399.abstract
AB When adequate levels of tyramine are maintained in the heart for a prolonged period (4 hr), this amine produces an almost complete depletion of heart norepinephrine. The results indicate that this depletion is due to a rapid decrease of norepinephrine from an easily releasable pool and then a slower release from a second pool, probably in equilibrium with the first. The administration of B.W. 392C60, a compound which produces an adrenergic neurone blockade, prevents norepinephrine depletion caused by guanethidine, slows the depletion caused by reserpine but does not affect that elicited by tyramine. The possibility is suggested that tyramine and guanethidine act on different stores of norepinephrine which are in equilibrium so that the depletion of one ultimately leads to the depletion of the other. Results are presented which show that the effect of monoamine oxidase inhibitors and adrenergic neurone blocking agents on the depletion of norepinephrine by guanethidine, reserpine and tyramine is the same. This finding suggests a similar mechanism for the hypotensive action of monoamine oxidase inhibitors and adrenergic neurone blocking drugs. The Williams & Wilkins Company