Cm. Stein et al., Basal and stimulated sympathetic responses after epinephrine - No evidenceof augmented responses, HYPERTENSIO, 32(6), 1998, pp. 1016-1021
Citations number
28
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
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.