• The Korean Journal of Physiology and Pharmacology
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• v.3 no.3
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• pp.339-350
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• 1999

The present study was attempted to examine the effect of pituitary adenylate cyclase-activating polypeptide (PACAP) on catecholamine (CA) secretion evoked by cholinergic stimulation, membrane depolarization and calcium mobilization from the isolated perfused rat adrenal gland. The perfusion of PACAP (10 nM) into an adrenal vein for 60 min produced a great inhibition in CA secretion evoked by ACh $(5.32{\times}10^{-3}\;M),$ high $K^+\;(5.6{\times}10^{-2}\;M),$ DMPP $(10^{-4}\;M\;for\;2\;min),$ McN-A-343 $(10^{-4}\;M\;for\;2\;min),$ cyclopiazonic acid $(10^{-5}\;M\;for\;4\;min)$ and Bay-K-8644 $(10^{-5}\;M\;for\;4\;min).$ Also, in the presence of neuropeptide (NPY), which is known to be co-localized with norepinephrine in peripheral sympathetic nerves, 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 PACAP (10 nM) under the presence of VIP antagonist $[(Lys^1,\;Pro^{2.5},\;Arg^{3.4},\;Tyr^6)-VIP\;(3\;{\mu}M)]$ for 20 min, CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were not altered greatly in comparison to the case of PACAP-treatment only. Taken together, these results suggest that PACAP causes the marked inhibition of CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization, indicating that this effect may be mediated by inhibiting influx of extracellular calcium and release in intracellular calcium in the rat adrenomedullary chromaffin cells.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.3
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• pp.259-270
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• 2001

The present study was attempted to investigate the characteristics of epibatidine on secretion of catecholamines (CA) from the isolated perfused model of the rat adrenal gland, and to establish the mechanism of action. Epibatidine $(3{\times}10^{-8}\;M)$ injected into an adrenal vein produced a great inhibition in secretory response of CA from the perfused rat adrenal gland. However, upon the repeated injection of epibatidine $(3{\times}10^{-8}\;M)$ at 15 min-intervals, CA secretion was rapidly decreased after second injection of epibatidine. However, there was no statistical difference between CA secretory responses of both 1st and 2nd periods by the successive administration of epibatidine at 120 min-intervals. Tachyphylaxis to releasing effects of CA evoked by epibatidine was observed by the repeated administration. Therefore, in all subsequent experiments, epibatidine was not administered successively more than twice only 120 min-intervals. The epibatidine-induced CA secretion was markedly inhibited by the pretreatment with atropine, chlorisondamine, pirenzepine, nicardipine, TMB-8, and perfusion of $Ca^{2+}-free$ Krebs solution containing EGTA, while was not affected by diphenhydramine. Moreover, the CA secretion evoked by ACh for 1st period $(0{\sim}4\;min)$ was greatly potentiated by the simultaneous perfusion of epibatidine $(1.5{\times}10^{-8}\;M),$ but followed by time-dependently gradual reduction after 2nd period. The CA release evoked by high potassium $(5.6{\times}10^{-8}\;M),$ for 1st period $(0{\sim}4\;min)$ was also enhanced by the simultaneous perfusion of epibatidine, but those after 2nd period were not affected. Taken together, these experimental data suggest that epibatidine causes catecholamine secretion in a calcium dependent fashion from the perfused rat adrenal gland through activation of neuronal cholinergic (nicotinic and muscarinic) receptors located in adrenomedullary chromaffin cells. It also seems that epibatidine-evoked catecholamine release is not relevant to stimulation of histaminergic receptors.

• Journal of Preventive Medicine and Public Health
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• v.20 no.2 s.22
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• pp.215-220
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• 1987

Under the extreme change of the environment, animals react physiologically to adapt to the stress and secrete catecholamines. Cold exposure is a kind of the environmental stress. Author tried to determine the amount of catecholamines in rat urine as a parameter of physiological response to cold stress. Urinary catecholamine was measured by using HPLC with fluorescence detector, cation exchange column prepacked with Bio·Rex 70 and ammonium pentaborate as catecholamine eluent. The amount of dopaminc in normal state rat urine was 42.0 ng, but under the low temperature of $5^{\circ}C$, the dopamine amount was increased to 221.25 ng/5 ml. Above findings are suggesting that catecholamine secretion, especially dopamine, increases in the stressful condition such as cold exposure.

• Proceedings of the PSK Conference
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• 2000.04a
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• pp.104.2-104.2
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• 2000

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.106.1-106.1
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• 2002

• Proceedings of the Korean Biophysical Society Conference
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• 2003.06a
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• pp.51-51
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• 2003

The medicinal plant Cimicifuga Racemosa (Black cohosh) has been used to treat many kinds of neuronal and menopausal symptoms, such as arthritis, menopausal depression, nerve pain, etc. Here, we examined the effect of Cimicifugoside (CF), one of triterpene glycosides which have been known as pharmacologically active ingredients of C. Racemosa, on nicotinic acetylcholine receptor (nAChR)-mediated catecholamine (CA) secretion in bovine adrenal chromaffin cell. Cimicifugoside inhibited calcium increase induced by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), a nAChR agonist with a half maximal inhibitory concentration (IC50) of 18${\pm}$2${\mu}$M. In contrast, cimicifugoside did not affect the calcium increases evoked by high K$\^$+/, veratridine, and bradykinin. The DMPP-induced sodium increase was also inhibited by cimicifugoside with IC50 of 2${\pm}$0.3${\mu}$M, suggesting that the activity of nAChRs is inhibited by cimicifugoside. Cimicifugoside did not effect on the KCl-induced secretion but markedly inhibited the DMPP-induced catecholamine secretion which was monitored by carbon-fiber amperometry in real time, and by high performance liquid chromatography (HPLC) through electrochemical detection. The results suggest that cimicifugoside selectively inhibits nAChR-mediated response in bovine chromaffin cells.

• Archives of Pharmacal Research
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• v.28 no.8
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• pp.914-922
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• 2005

The present study was designed to examine the effects of green tea extract (CUMC6335) and epigallocatechin gallate (EGCG) on secretion of catecholamines (CA) in the isolated perfused rabbit adrenal gland. In the presence of CUMC6335 $(200 {\mu}g/mL)$ into an adrenal vein for 60min, CA secretory responses evoked by ACh (5.32 mM), high $K^+$ (56 mM), DMPP $(100{\mu}M \;for\;2min)$, and Bay-K-8644 $(10{\mu}M\;for\;4min)$ from the isolated perfused rabbit adrenal glands were greatly inhibited in a time-dependent fashion. However, EGCG $(10{\mu}g/mL)$ did not affect CA release evoked by ACh, high $K^+$, and Bay-K-8644. CUMC6335 itself failed to affect basal catecholamine output. Taken together, these results demonstrate that CUMC6335 inhibits CA secretion evoked by stimulation of cholinergic nicotinic receptors, as well as the direct membrane depolarization from the isolated perfused rabbit adrenal gland. It is thought that this inhibitory effect of CUMC6335 may be due at least in part to the blocking action of the L-type dihydropyridine calcium channels in the rabbit adrenomedullary chromaffin cells, which is relevant to the cholinergic nicotinic blockade. It seems that there is a big difference in mode of action between CUMC6335 and EGCG.

• Archives of Pharmacal Research
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• v.14 no.1
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• pp.55-67
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• 1991

The influence of caffeine on secretion of catecholamines (CA) was examined in the isolated perfused rat adrenal gland. Caffeine (0.3 mM) perfused into an adrenal vein of the gland produced a marked increase in secretion of CA. This secretory effect of CA evoked by perfusion of caffeine for one minute was considerably prolonged, lasting for more than 90 minutes. The tachyphylaxis to releasing effect of CA induced by caffeine was observed by repeated perfusion of this drug. The caffeine-evoked CA secretion was markedly inhibited by pretreatment with ouabain, trifluoperazine, TMB-8 and perfusion with calcium-free Krebs solution containing 5 mM EGTA, but was not affected by perfusion of calcium-free Krebs solution without other addition. CA secretion evoked by caffeine was not reduced significantly by pretreatment with chlorisondamine but after the first collection of perfusate for 3 min was clearly inhibited. Interestingly, the caffeine-evoked CA secretion was considerably potentiated by pretreatment with atropine or pirenzepine, but after the first collection for 3 min it was markedly decreased. These experimental results suggest that caffeine causes a marked increase in secretion of CA from the isolated perfused rat adrenal gland by an extracellular calcium-independent exocytotic mechanism. The secretory effect of caffeine may be mainly due to mobilization of calcium from an intracellular calcium pool in the rat chromaffin cells and partly due to stimulation of both muscarinic and nicotinic receptors.

• Biomolecules & Therapeutics
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• v.11 no.1
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• pp.33-40
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• 2003

The present study was designed to investigate the effects of green tea extract (CUMC6335) and epigallocatechin gallate (EGCG) on secretion of catecholamines (CA) in the isolated perfused rat adrenal gland. ill the presence of CUMC6335 (100 $\mu\textrm{g}$/mL) into an adrenal vein for 60 min, CA secretory responses evoked by ACh(5.32 mM), high $K^+$ (56 mM) and Bay-K-8644 (10$\mu$M for 4 min) from the isolated perfused rat adrenal glands were greatly inhibited in a time-dependent fashion. However, EGCG (8 $\mu\textrm{g}$/mL) did not affect CA release evoked by ACh, high $K^+$ and Bay-K-8644. CUMC6335 itself did fail to affect basal catecholamine output. Taken together, these results demonstrate that CUMC6335 inhibits greatly CA secretion evoked by stimulation of cholinergic nicotinic receptors as well as by the direct membrane deplarization from the isolated perfused rat adrenal gland. It is felt that this inhibitory effect of CUMC6335 may be due to blocking action of the L-type dihydropyridine calcium channels in the rat adrenal medullary chromaffin cells, which is relevant to the cholinergic nicotinic blockade. It seems that there is a big difference in mode of action between CUMC6335 and EGCG.

• The Korean Journal of Pharmacology
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• v.27 no.2
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• pp.167-181
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• 1991

The present study was an attempt to investigate the effect of forskolin on secretion of catecholamines (CA) evoked by Ach, excess $K^+$, DMPP, McN-A-343 and caffeine from the isolated perfused rat adrenal glands and to elucidate its mechanism of action. The perfusion with forskolin (1.0 uM) for 1 min into the adrenal vein enhanced markedly the secreation of CA evoked by Ach (50 ug), excess $K^+$ (56 mM) DMPP (100 uM) and by caffeine (0.3 mM) but did not that by McN-A-343. Forskolin alone did not potentiate the CA secretion. Moreover, forskolin augmented the CA release evoked by the above same stimulation even in the absence of extracellular calcium. The 1 min perfusion of 300 uM-dibutyryl cyclic AMP (DBcAMP), which is known to increase cyclic AMP levels, led to enhancement of Ca secretion evoked by Ach, excess $K^+$ and DMPP but did not that by McN-A-343 and caffeine. DBcAMP by itself also did not augment the CA secretion. In the calcium-free medium DBcAMP significantly enhanced the CA secretion by the same stimulation, except for the case of McN-A-343. These experimental results suggest that forskolin activates adenylate cyclase, resulting the elevation of cyclic AMP which may potentiate cholinergic nicotinic receptor-mediated and also depolarization-dependent CA secretion and that it may alter the intracellular calcium homeostasis in the rat adrenal glands.