Basal and stimulated sympathetic responses after epinephrine - No evidenceof augmented responses

Delayed facilitation of norepinephrine release through the action of epinep hrine (NE) at presynaptic P-adrenoceptors has been postulated to account fo r the delayed hemodynamic effects of epinephrine and to be a mechanism caus ally related to the development of hypertension. To determine whether a sho rt-term increase in epinephrine concentrations resulted in subsequent facil itation of sympathetic responses, 9 healthy subjects (age, 21+/-0.9 years) were studied at rest and during physiological stress on 2 occasions when th ey received an infusion of either saline or epinephrine (20 ng/kg per minut e) in random order. Heart rate, blood pressure, forearm blood flow, epineph rine concentrations, and NE spillover were measured at rest, during mental stress (Stroop test), and during a cold presser test. Measurements were per formed before, during the 1-hour infusion of epinephrine or placebo, and 1 hour after the infusion. A radioisotope dilution method was used to measure NE spillover. Hemodynamic measurements and NE spillover were increased dur ing the infusion of epinephrine, but 1 hour after discontinuation of epinep hrine there was no significant augmentation of hemodynamic or sympathetic r esponses. NE spillover 1 hour after saline or epinephrine infusion was simi lar (0.85+/-0.2 versus 0.87+/-0.2 mu g/min; P=0.92). In addition, there was no delayed facilitation of stress-induced hemodynamic or NE responses afte r epinephrine. These findings do not support the hypothesis that epinephrin e results in delayed facilitation of NE release.