AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 6 1431-R1437, Copyright © 1991 by American Physiological Society
Mechanisms involved in the rapid dissipation of plasma epinephrine response to bacterial endotoxin in conscious rats
M. Qi, Z. Z. Zhou, R. D. Wurster and S. B. Jones
Department of Physiology, Loyola University Medical Center, Maywood, Illinois 60153.
Conscious rats treated with bolus endotoxin (ET; 4.0 mg/kg) increased
plasma epinephrine (Epi) 48-fold (from 134 +/- 5 to 6,545 +/- 1,607 pg/ml)
at 30 min, but by 6 h this elevation was less than 9-fold above control
(1,174 +/- 166 pg/ml). In contrast, plasma norepinephrine (NE) elevation
(6.5-fold above control) was maintained during the protocol. The present
study was designed to test the hypothesis that the decreased Epi response
following ET was due to 1) depletion of adrenal Epi content such that
adrenomedullary stimulation would not release Epi, 2) decreased Epi release
with direct stimulation, i.e., desensitization of release, or 3) decreased
afferent signals generated by ET itself. In these experiments an initial
low ET dose (0.5 mg/kg) was followed 3 h later by a second dose of either
the same (0.5 mg/kg) or greater (4.0 mg/kg) magnitude. Plasma Epi was
elevated following the initial (low) dose but not following the same second
(0.5 mg/kg) dose, whereas the second higher dose (4.0 mg/kg) resulted in
elevated plasma Epi. This response to high dose was 60% less than that
observed with 4.0 mg/kg as an initial dose. Just before the second ET
bolus, there was no depletion of adrenal Epi content (P greater than 0.05
saline vs. ET treated), and direct nerve stimulation demonstrated enhanced
rather than attenuated Epi release from the adrenal medulla (P less than
0.05 saline vs. ET treated). These results suggest that the decline in Epi
following the ET-induced elevation may be mediated by a decrease in the
afferent signal that initiates Epi release.
