The differential effects of hypothermia suggest that sympathomimetic amines release norepinephrine via mechanisms distinct from depolarization-induced release.
Animal data on hypothermia's selective effects leave open distinct amine- versus nerve-evoked norepinephrine release mechanisms; human relevance remains untested.
The effects of hypothermia on the sympathetic neuroeffector junction were studied in the isolated perfused cat spleen. The experiments were aimed at determining the temperature dependence both of prejunctional events, i.e., efflux of norepinephrine from the sympathetic nerves in response to electrical stimulation or to indirectly acting sympathomimetic amines like tyramine or phenethylamine, and of postjunctional events, i.e., the contractile response of the smooth muscle to the norepinephrine liberated. Hypothermia was found to depress both the norepinephrine efflux in response to stimulation and the contractile response to the endogenous norepinephrine released, as well as to exogenous norepinephrine. However, these processes were found to respond differently to temperature change. Thus hypothermia depressed norepinephrine release as well as the pressor responses to tyramine and phenethylamine much more strongly than the corresponding responses to electrical nerve stimulation or the pressor response to exogenous norepinephrine. The results strongly support the concept that sympathomimetic amines release norepinephrine from sympathetic nerves by mechanisms which differ from those mediating norepinephrine release induced by depolarization.
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Wennmalm et al. (1970) studied this question.
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