Processes that interfere locally with the inactivation of circulating epinephrine by binding in sympathetic nerve endings potentiate its effects on regional perfusion.
These rat perfusion shifts warrant no clinical extrapolation; leaves open human relevance of local epinephrine inactivation.
The intravenous administration of 1 µg l-epinephrine increases the fraction of the cardiac output, measured by K42 uptake, which is delivered to the rat heart. This effect of the catecholamine is potentiated in hyperthyroidism or by a single injection of cocaine. One microgram of epinephrine causes no change in the fractional perfusion of the innervated rat salivary gland, but produces a marked decrease following chronic sympathetic denervation. Processes which interfere locally with the inactivation of circulating epinephrine by binding in sympathetic nerve endings thus potentiate its effects on regional perfusion.
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Wurtman et al. (1964) studied this question.
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