Korean J Intern Med.
1997 Jun;12(2):163-175.
Influence of pentobarbital-Na on stimulation-evoked catecholamine secretion in
the perfused rat adrenal gland
- Affiliations
-
- 1Department of Pharmacology and Internal Medicine, College of Medicine, Chosun
University, Kwangju, Korea.
Abstract
OBJECTIVES
The present study was attempted to investigate the effects of
pentobarbital-Na, one of the barbiturates which are known to depress excitatory
synaptic transmission in the central nervous system at concentrations similar to
those required for the induction and maintenance of anesthesia, on
catecholamines (CA) secretion evoked by cholinergic stimulation and
membrane-depolarization from the isolated perfused rat adrenal gland, and to
clarify the mechanism of its action. METHODS: Mature male Sprague-Dawley rats
were anesthetized with thiopenal-Na (40 mg/kg, s.c.). The adrenal gland was
isolated by the methods of Wakade. A cannula used for perfusion of the adrenal
gland was inserted into the distal end of the renal vein. The adrenal gland was
carefully removed from the animal and placed on a platform of a leucite chamber.
RESULTS: The perfusion of pentobarbital-Na(30-300 uM) into an adrenal vein for
20 min produced relatively dose-dependent inhibition in CA secretion evoked by
ACh(5.32 mM), DMPP(100 uM for 1 min), McN-A-343(200 uM for 2 min), Bay-K-8644(10
uM) and high potassium(56 mM), while it did not affect the CA secretion of
cyclopiazonic acid(10 uM). Also, in the presence of thiopental-Na (100 uM), CA
secretory responses evoked by ACh, DMPP, McN-A-343 and high K+ were markedly
depressed. Moreover, in adrenal glands preloaded with ketamine(100 uM for 20
min), which is known to be a dissociative anesthetic, CA secretion evoked by
ACh, DMPP, McN-A-343 and high K+ were significantly attenuated. CONCLUSION:
Taken together, these experimental results suggest that pentobarbital-Na
depresses CA release evoked by both cholinergic stimulation and
membrane-depolarization from the isolated rat adrenal medulla and that this
inhibitory activity may be due to the result of the direct inhibition of Ca++
influx into the chromaffin cells without any effect on the calcium mobilization
from the intracellular store.