A comparison of the indirect sympathomimetic actions of tyramine and acetaldehyde in isolated smooth muscle preparations

Abstract

Rat vas deferens and rabbit aortic strips were used in the present study to compare and contrast the mechanism by which tyramine and acetaldehyde produce contration in smooth muscle. Tetrodotoxin abolished contractile responses in rat vas deferens induced by transmural stimulation, but not by addition of tyramine or acetaldehyde. This indicated that the ability of tyramine and acetaldehyde to produce contraction does not depend upon propagation of the nerve impulse. The ability of acetaldehyde to release transmitter from the tissue was also studied and compared to tyramine in isolated rabbit aortae previously exposed to [ 14C]norepinephrine. Omitting calcium from the bathing solution did not alter the ability of either agent to release radioactivity from aortae. Similar amounts of [ 14C]norepinephrine and 14C-deaminated metabolites were recovered from the efflux media during exposure to acetaldehyde and tyramine. This finding suggests that these agents utilize the same pool of endogenous transmitter to produce their sympathomimetic effects. On the other hand, differences were found in the manner in which tyramine and acetaldehyde gain access to transmitter stores. The ability of tyramine to increase loss of radioactivity from aortae was antagonized by exposure of tissues to cocaine, ouabain, and cold (4°C). Acetaldehyde-evoked loss of radioactivity was not altered by these procedures. Whereas it is clear that tyramine utilizes the neuronal uptake mechanism, acetaldehyde appears to diffuse across the membrane by virtue of its lipid solubility in order to gain access to the same tissue transmitter storage sites.