• Journal of Preventive Medicine and Public Health
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• v.26 no.4 s.44
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• pp.565-573
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• 1993

Noise is not only affecting the ear and the auditory cortex locally, but its influence is widely spread throughout the brain structures, e. g., the reticular formation, the brain stem nuclei or the subcortical forebrain area. Hence, any of the organism's activities can be hindered or stimulated by noise. High noise is a stressor and the catecholamine level can be used both as a stress marker and as an indicator of modified sympathetic nervous system activity. Several recent studies have found that the urinary excretion of catecholamines is increased due to high noise intensity, especially unexpectedly high and long lasting noise. The present study was conducted in order to examine the effects of noise stress on urinary excretion of ctecholamines in rats and humans. Rats were exposed to 90 dB noise for 10, 30, and 60 minutes, 3 and 12 hours. 24 hour . urinary samples were collected and the catecholamones were extracted by alumina and analyzed by HPLC-ECD. Catecholamine levels increased with time of exposure up to 60 minutes : norepinephrine concentration at 60 min of noise=1.038 ng/ml, epinephrine=0.636 ng/ml. Urine catecholamines of blue collar workers exposed to 90 dB of noise at the work place were collected between 2 and 4 p.m. and compared to that of white collar workers exposed to 70 dB. Mean norepinephrine level of the blue collar workers was 0.89 ng/ml (${\pm}0.25$), epinephrine 0.24ng/m1 (${\pm}0.09$), and that of the white collar workers 0.48 ng/ml (${\pm}0.12$), epinephrine 0.19 ng/ml(${\pm}0.05$). It was concluded that noise acts as a stressor and increases the catecholamine levels in both rats and humans.

• Archives of Pharmacal Research
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• v.28 no.6
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• pp.699-708
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• 2005

The present study was designed to investigate the effect of naloxone, a well known opioid antagonist, on the secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane-depolarization in the isolated perfused rat adrenal glands, and to establish its mechanism of action. Naloxone ($10^{-6}\~10^{-5}$ M), perfused into an adrenal vein for 60 min, produced dose- and time-dependent inhibition of CA secretory responses evoked by ACh ($5.32\times10^{-3}$ M), high K+ ($5.6\times10^{-2}$ M), DMPP ($10^{-4}$ M) and McN-A-343 ($10^{-4}$ M). Naloxone itself also failed to affect the basal CA output. In adrenal glands loaded with naloxone ($3\times10^{-6}$ M), the CA secretory responses evoked by Bay-K-8644, an activator of L-type $Ca^{2+}$ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}$-ATPase, were also inhibited. In the presence of met-enkephalin ($5\times10^{-6}$ M), a well known opioid agonist, the CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly inhibited. Taken together, these results suggest that naloxone greatly inhibits the CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that these inhibitory effects of naloxone does not involve opioid receptors, but might be mediated by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of $Ca^{2+}$ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself.

• Archives of Pharmacal Research
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• v.12 no.3
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• pp.166-175
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• 1989

In the previous observations, it was reported that both total ginseng saponin and panaxadiol revealed the marked secretory effect of catecholamines (CA) from the rabbit adrenal gland and that CA secretion induced by them is due to dual mechanisms, cholinergic action and the direct action. In the present study, an attempt to investigate the effect of panaxatriol-type saponin (PT), which is known as an active component of Korean ginseng, on the secretion of CA from the rabbit adrenal gland was made. PT(200 $\mu$g) administered into adrenal vein evoked significantly secretion of CA from the isolated perfused rabbit adrenal gland. Secretory effect of CA produced by PT was attenuated clearly by treatment with chlorisondamine or adenosine, but was markedly increased by physostigmine. Perfusion of Krebs solution containing PT (200 $\mu$g) for 30 min potentiated greatly secretion of CA induced by acetylcholine. PT-induced CA secretion was weakened considerably by ouabain treatement or perfusion of calcium-free Krebs solution. These experimental data demonstrate that PT releases CA from the isolated perfused rabbit adrenal gland by a calcium-dependentd exocytotic mechanism. It seems that the secretory effect of PT is caused through the release of acetylcholine form cholinergic terminals present in the adrenal gland and a direct action on the chromaffin cell itself.

• The Korean Journal of Zoology
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• v.38 no.4
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• pp.498-504
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• 1995

The effeds of riboflavin defidency on the biosynthesis of flavin pepddes and levels of flavoenzymes and catecholamines have been investigated. The percentage of 14C. riboflavin radioactivity formed in mitochondria appeared to increase up to 2 weeks but started to decline at 3 weeks. A significant increase of radioactivity incorporation into mitochondria and into trypsin-digestable plus trypsin-non-digestibie flavin peptides was detected in riboflavin-deficient animals. More than 35% of incorporation was observed at the end of the first week and 160% higher incorporation was observed in fiavin peptide after the second week. Activities of MAO and succinate dehydrogenase were affected markedly by riboflavin status whereas those of acetyichoilnesterase were not affected. Riboflavin defidency also brought about marked reductions in levels of epineplrrine and norepinephrine. it is concluded that the levels of flavin peptides, MAO and succinate dehydrogenase, and catecholamines were affected significanily by the availability of riboflavin and in particular the duration of its depiction.

• Archives of Pharmacal Research
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• v.25 no.4
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• pp.511-521
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• 2002

The purpose of this study was to determine whether bromocriptine affects the catecholamines (CA) secretion evoked in isolated perfused rat adrenal glands, by cholinergic stimulation, membrane depolarization and calcium mobilization, and to establish the mechanism of its action. The perfusion of bromocriptine ($1~10{\;}{\mu}M$) into an adrenal vein, for 60 min, produced relatively dose-dependent inhibition in the secretion of catecholamines (CA) evoked by acetylcholine (ACh, 5.32 mM), DMPP ($100{\;}{\mu}M$ for 2 min), McN-A-343 ($100{\;}{\mu}M$ for 2 min), cyclopiazonic acid (CPA, $10{\;}{\mu}M$ for 4 min) and Bay-K-8644 ($10{\;}{\mu}M$ for 4 min). High $K^+$ (56 mM)-evoked CA release was also inhibited, although not in a dose-dependent fashion. Also, in the presence of apomorphine ($100{\;}{\mu}M$), which is also known to be a selective $D_2$-agonist, the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly depressed. However, in adrenal glands preloaded with bromocriptine ($3{\;}{\mu}M$) in the presence of metoclopramide ($15{\;}{\mu}M$), a selective $D_2$-antagonist, the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid considerably recovered as compared to that of bromocriptine only. Taken together, these results suggest that bromocriptine can inhibit the CA secretion evoked by stimulation of cholinergic receptors, as well as by membrane depolarization, in the perfused rat adrenal medulla. It is thought this inhibitory effect of bromocriptine may be mediated by inhibiting the influx of extracellular calcium and the release from intracellular calcium stores, through the activation of dopaminergic $D_2$-receptors located in the rat adrenomedullary chromaffin cells. Furthermore, these findings also suggest that the dopaminergic $D_2$-receptors may play an important role in regulating adrenomedullary CA secretion.

• Development and Reproduction
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• v.27 no.4
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• pp.213-220
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• 2023

Previously, we showed that a chronic-low-dose nonylphenol (NP) exposure resulted in histological changes with sexually dimorphic pattern in rat adrenal glands. We hypothesized that such structural changes are closely related to the hormonal secretory patterns. To test this hypothesis, we developed the short-term adrenal incubation method, and measured the levels of catecholamines and cortical steroids using the high-performance liquid chromatography with electrochemical detection (HPLC-ECD) and specific enzyme-linked immunosorbent assay, respectively. The norepinephrine (NE) levels in media from NP-treated female adrenal, except 100 pM NP, were significantly increased [control (CTL) vs 1 nM NP, p<0.001; vs 10 nM NP, p<0.05; vs 100 nM NP, p<0.001; vs 1 µM NP, p<0.01]. The NE secretion from male adrenal was higher when treated with 100 nM and 1 µM NP (CTL vs 100 nM NP, p<0.05; vs 1 µM NP, p<0.05, respectively). The aldosterone level in the female adrenal media treated with 100 pM NP was significantly decreased, on the other hand, that of media treated with 10 nM NP was significantly increased (CTL vs 100 pM NP, p<0.05; vs 10 nM NP, p<0.01). In male adrenal media, the aldosterone levels of 10 nM, 100 nM and 1 µM NP-treated media were significantly declined (CTL vs 10 nM NP, p<0.001; vs 100 nM NP, p<0.001; vs 1 µM NP, p<0.001). These results showed the NP treatment altered secretory pattern of aldosterone from adrenals of both sexes, showing sexual dimorphism. It may be helpful for understanding possible adrenal pathophysiology, and endocrine disrupting chemicals-related sexually dimorphic phenomena in adrenals.

• BMB Reports
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• v.31 no.3
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• pp.264-268
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• 1998

Dopamine (DA) acts on swimming motor neurons (SMNs) of Polyorchis penicillatus as an inhibitory neurotransmitter by hyperpolarizing their membrane potentials, which results from the activation of voltagesensitive potassium channels mediated through a $D_2-type$ receptor. In addition, DA, and not the hyperpolarized membrane potential, directly decreased the input resistance of SMNs by ca. 50% from 1.42 to 0.68 $G{\Omega}$. It strongly indicates that DA can shunt other excitatory synaptic signals onto SMNs where DA usually elicited much greater responses in their neurites than soma. All these evidences suggest that DA may operate in this primitive nervous system in dual modes as an inhibitory neurotransmitter and neuromodulator as well.

• BMB Reports
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• v.28 no.4
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• pp.323-330
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• 1995

Recent studies have shown that dopamine applied to cultured swimming motor neurons of Polyorchis penicillatus produces an inhibitory action by opening potassium channels through $D_2$-like receptors. In this study, it was demonstrated that dopamine found in the hydromedusa was not from exogenous sources and the content of dopamine depended on the $Ca^{2+}$ content of the dissecting media. In addition, a combination of thin layer chromatography and high performance liquid chromatography showed the presence of DOPA and DO PAC-like compounds in the jellyfish. The glyoxylic acid method for catecholamines suggested that a population of small cells, neither swimming motor neurons nor B-like neurons, had dopaminergic systems. From all these results, it is suggested here that DA synthesized from DOPA in some cells is released. being dependent on calcium concentrations, into a synaptic cleft and degraded into DOPAC after acting as an inhibitory transmitter to swimming motor neurons.

• Biomolecules & Therapeutics
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• v.3 no.1
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• pp.28-33
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• 1995

Effects of Ginkgo biloba leaf extract (GBE) and its components kaempferol-coumaroyl glucosyl rhamnoside (Kc), quercetin-coumaroyl glucosyl rhamnoside (Qc), ginkolide (G) and bilobalide (B) on blood pressure and on the levels of neurotransmitters in the spontaneously hypertensive rat brain were examined. Blood pressure decreased about 10 mmHg after administration of GBE but without significance. The concentration of norepinephrine increased (3 times) and that of DOPAC was decreased (38%) after administration of Qc. And 3-MT concentration was increased (36%) by Kc administration in striatum. While Qc administration increased the concentration of Ach (260%) and Ch(29%) significantly, B administration increased Ch concentration in cerebral cortex.

• BMB Reports
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• v.29 no.2
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• pp.151-155
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• 1996

To swimming motor neurons (SMNs) of Polyorchis penicillatus, a hydrozoan medusae, dopamine (DA) acts as an inhibitory neurotransmitter by hyperpolarizing its membrane potential and decreasing its firing rate as well. Such an inhibitory action of DA is caused by an increased permeability to potassium (K) ions. To investigate whether voltage-gated K channels are directly responsible for the membrane hyperpolarization induced by DA, we employed whole-cell voltage clamp configuration. One ${\mu}M$ DA applied to SMNs increased the peak and rear values of voltage-gated K currents by 37 and 54%, respectively, in a reversible manner. Combined with subtraction analysis, this result suggests that the outflux of K ions by DA in SMNs occurs mainly through rectifier-like K channels.