Y. Takauchi et al., Tyramine-induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats, ACT PHYSL S, 168(2), 2000, pp. 287-293
With the use of dialysis technique, the effects of tyramine on in situ card
iac sympathetic nerve endings were examined in anaesthetized cats. Dialysis
probes were implanted in the left ventricular myocardium, and the concentr
ation of dialysate noradrenaline (NA) served as an indicator of NA output a
t the cardiac sympathetic nerve ending. Locally applied tyramine (600 mu M)
increased dialysate NA levels from 17 +/- 1 (pg mL(-1)) to 3466 +/- 209 (p
g mL(-1)). Pretreatment with reserpine (vesicle transport NA blocker 1 mu M
) did not affect tyramine-induced NA efflux. The tyramine-induced NA efflux
was augmented by pretreatment with pargyline (1 mM) but suppressed by parg
yline (10 mM). Pretreatment with alpha-methyl-tyrosine suppressed NA efflux
evoked by tyramine. These pretreatments did not affect the time course of
NA efflux but only altered peak height of NA efflux. The efflux of NA evoke
d by tyramine was not associated with any reduction of dihydroxyphenylglyco
l (DHPG). In contrast, in the pretreatment with reserpine, the efflux of NA
was associated with a reduction of DHPG. This result suggests that NA grad
uation between axoplasm and stored vesicle contributes to maintaining the a
xoplasmic NA level during carrier-mediated outward NA transport. The tyrami
ne-induced NA efflux provides a close reflection of the NA content at the n
erve ending. With the use of dialysis, this experimental model is suitable
for studying the mechanism of sympathomimetic amine-induced neurotransmitte
r efflux.