• The Korean Journal of Pharmacology
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• v.29 no.2
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• pp.183-188
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• 1993

Effects of glucose on the catecholamine release from the hypothalamic fragments in vitro were studied. Basal release of catecholamines was inversely related to the concentrations $(5{\sim}30\;mM)$ of glucose in the incubation medium. Glucose did not affect the 30 mM $K{^+}-stimulated$ release of catecholamine. In the presence of tetrodotoxin $(10\;{\mu}M)$, the inhibitory effect of glucose on the basal release of catecholamines was largely persisted, but the inhibitory effect of 30 mM glucose on dopamine release was largerly blocked. In the presence of both tetrodotoxin $(10\;{\mu}M)$ and desipramine $(3\;{\mu}M)$, glucose failed to affect the basal catecholamine release. The results suggest that glucose modulates the catecholamine release through a direct action on the catecholaminergic nerve terminals, as well as through a trans-synaptical action. The glucose-modulation of the catecholamine release may explain, at least in part, the diabetes-induced changes in the hypothalamic catecholamine metabolism.

• The Korean Journal of Pharmacology
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• v.8 no.2
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• pp.41-47
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• 1972

Fluorides were supposed to exert a stimulatory action on the catecholamine release. In this study, the authors attempted to investigate the action of sodium fluoride on the catecholamine release from the isolated perfused cow adrenal gland and rat heart. And also the inhibitory effect of sodium fluoride on the monoamine oxidase activity in rat heart and liver mitochondria was investigated. The monoamine oxidase activity was measured by the conversion of benzylamine to benzaldehyde. The results obtained were follows; 1. Sodium fluoride stimulated the release of catecholamine from the isolated perfused cow adrenal gland and rat heart. 2. Sodium fluoride inhibited the rat heart and liver mitochondrial monoamine oxidase activity.

• Archives of Pharmacal Research
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• v.25 no.6
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• pp.932-939
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• 2002

The aim of the present study was to determine the characteristics of cytisine on the secretion of catecholamines (CA) in isolated perfused rat adrenal glands, and to clarify its mechanism of action. The release of CA evoked by the continuous infusion of cytisine ($1.5{\times}10^{-5} M$) was time-dependently reduced from 15 min following the initiation of cytisine infusion. Furthermore, upon the repeated injection of cytisine ($5{\times}10^{-5}$), at 30 min intervals into an adrenal vein, the secretion of CA was rapidly decreased following the second injection. Tachyphylaxis to the release of CA was observed by the repeated administration of cytisine. The cytisine-induced secretion of CA was markedly inhibited by pretreatment with chlorisondamine, nicardipine, TMB-8, and the perfusion of $Ca^{2+}$-free Krebs solution, while it was not affected by pirenzepine or diphenhydramine. Moreover, the secretion of CA evoked by ACh was time-dependently inhibited by the prior perfusion of cytisine ($5{\times}10^{-6} M$). Taken together, these experimental data suggest that cytisine causes secretion of catecholamines from the perfused rat adrenal glands in a calcium-dependent fashion through the activation of neuronal nicotinic ACh receptors located in adrenomedullary chromaffin cells. It also seems that the cytisine-evoked release of catecholamine is not relevant to the activation of cholinergic M$_1$-muscarinic or histaminergic receptors.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.87.2-88
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• 2003

The present study was conducted to investigate the effects of pinacidil, a potassium channel opener, on arterial blood pressure, catecholamine release and vascular contractile responses in the normotensve rats and to establish the mechanism of action. Phenylephrine (an adrenergi $_1$-receptor agonist) and high potassium (a membrane- depolarizing agent) caused greatly contractile responses in the isolated aortic strips, respectively. These phenylephrine (10$\^$-5/ M)-induced contractile responses were dose-dependently depressed in the presence of pinacidil (25 ∼ 100 ${\mu}$M). (omitted)

• 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 Physiology and Pharmacology
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• v.2 no.6
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• pp.753-761
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• 1998

Preconditioning of a heart with small doses of catecholamines induces a tolerance against the subsequent lethal ischemia. The present study was performed to find a specific receptor pathway involved with the catecholamine preconditioning and to test if adenosine plays a role in this cardioprotective effect. Isolated rat hearts, pretreated with small doses of ${\alpha}-\;or\;{\beta}-adrenergic$ agonists/antagonists, were subjected to 20 minutes ischemia and 20 minutes reperfusion by Langendorff perfusion method. Cardiac mechanical functions, lactate dehydrogenase and adenosine release from the hearts were measured before and after the drug treatments and ischemia. In another series of experiments, adenosine $A_1\;or\;A_2$ receptor blockers were treated prior to administration of adrenergic agonists. Pretreatments of a ${\beta}-agonist,\;isoproterenol(10^{-9}{\sim}10^{-7}\;M)$ markedly improved the post-ischemic mechanical function and reduced the lactate dehydrogenase release. Similar cardioprotective effect was observed with an ?-agonist, phenylephrine pretreatment, but much higher $concentration(10^{-4}\;M)$ was needed to achieve the same degree of cardioprotection. The cardioprotective effects of isoproterenol and phenylephrine pretreatments were blocked by a ${\beta}_1-adrenergic$ receptor antagonist, atenolol, but not by an ${\alpha}_1-antagonist,$ prazosin. Adenosine release from the heart was increased by isoproterenol, and the increase was also blocked by atenolol, but not by prazosin. A selective $A_1-adenosine$ receptor antagonist, 1,3-dipropyl-8-cyclopentyl xanthine (DPCPX) blocked the cardioprotection by isoproterenol pretreatment. These results suggest that catecholamine pretreatment protects rat myocardium against ischemia and reperfusion injury by mediation of ${\beta}_1-adrenergic$ receptor pathway, and that adenosine is involved in this cardioprotective effect.

• The Korean Journal of Pharmacology
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• v.28 no.2
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• pp.181-190
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• 1992

The present study was conducted to investigate the effect of opioids on catecholamine (CA) secretion evoked by a selective cholinergic nicotinic agonist, 1,1-dimethyl-4-phenyl piperazinium (DMPP) and acetylcholine from the retrogradely perfused rat adrenal glands. Methionine-enkephalin $(9.68{\times}10^{-6}\;M)$ caused a significant inhibition of CA secretion evoked by DMPP (100 uM) and $ACh\;(50\;{\mu}g)$, but had no effect on the spontaneous (basal) CA release. Morphine $(1.73{\times}10^{-5}\;M)$ attenuated considerablely the increase in CA release induced by DMPP and ACh. Morphine itself also did not affect the basal CA output. A 20 to 65% reduction of the DMPP- and ACh-evoked increase in CA release was observed after the pretreatment with methionine-enkephalin or morphine. The increase in CA release evoked by DMPP and ACh was reduced markedly by preloading with an opiate antagonist naloxone $(1.22{\times}10^{-7}\;M)$ while basal CA output was not affected by naloxone. These present experimental results suggest that the nicotinic stimulation-evoked CA release from the perfused rat adrenal gland is inhibited by endogenously released opioid peptides through activation of opiate receptors located in the adrenal gland.

• Proceedings of the PSK Conference
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• 2001.10a
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• pp.146.3-147
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• 2001

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.1
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• pp.21-30
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• 2007

The present study was designed to establish comparatively the inhibitory effects of cilnidipine(CNP), nifedipine(NIF), and $\omega$-conotoxin GVIA(CTX) on the release of CA evoked by cholinergic stimulation and membrane depolarization from the isolated perfused model of the rat adrenal medulla. CNP(3 ${\mu}M$), NIF(3 ${\mu}M$), and CTX(3 ${\mu}M$) perfused into an adrenal vein for 60 min produced greatly inhibition in CA secretory responses evoked by ACh($5.32{\times}10^{-3}M$), DMPP($10^{-4}M$ for 2 min), McN-A-343($10^{-4}M$ for 2 min), high $K^+(5.6{\times}10^{-2}M)$, Bay-K-8644($10^{-5}M$), and cyclopiazonic acid($10^{-5}M$), respectively. For the CA release evoked by ACh and Bay-K-8644, the following rank order of potency was obtained: CNP>NIF>CTX. The rank order for the CA release evoked by McN-A-343 and cyclopiazonic acid was CNP>NIF>CTX. Also, the rank orders for high $K^+$ and for DMPP were NIF>CTX>CNP and NIF>CNP>CTX, respectively. Taken together, these results demonstrate that all voltage-dependent $Ca^{2+}$ channels(VDCCs) blockers of cilnidipine, nifedipine, and $\omega$-conotoxin GVIA inhibit greatly the CA release evoked by stimulation of cholinergic(both nicotinic and muscarinic) receptors and the membrane depolarization without affecting the basal release from the isolated perfused rat adrenal gland. It seems likely that the inhibitory effects of cilnidipine, nifedipine, and $\omega$-conotoxin GVIA are mediated by the blockade of both L- and N-type, L-type only, and N-type only VDCCs located on the rat adrenomedullary chromaffin cells, respectively, which are relevant to $Ca^{2+}$ mobilization. It is also suggested that N-type VDCCs play an important role in the rat adrenomedullary CA secretion, in addition to L-type VDCCs.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.4
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• pp.327-335
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• 2009

The aim of this study was to determine whether losartan, an angiotensin II (Ang II) type 1 ($AT_1$) receptor could influence the CA release from the isolated perfused model of the rat adrenal medulla. Losartan (5${\sim}$50 ${\mu}$M) perfused into an adrenal vein for 90 min produced dose- and time-dependent inhibition of the CA secretory responses evoked by ACh (5.32 mM), high $K^+$ (56 mM, a direct membrane depolarizer), DMPP (100 ${\mu}$M) and McN-A-343 (100 ${\mu}$M). Losartan failed to affect basal CA output. Furthermore, in adrenal glands loaded with losartan (15 ${\mu}$M) for 90 min, the CA secretory responses evoked by Bay-K-8644 (10 ${\mu}$M, an activator of L-type $Ca^{2+}$ channels), cyclopiazonic acid (10 ${\mu}$M, an inhibitor of cytoplasmic $Ca^{2+}$ -ATPase), veratridine (100 ${\mu}$M, an activator of $Na^+$ channels), and Ang II (100 nM) were markedly inhibited. However, at high concentrations (150${\sim}$300 ${\mu}$M), losartan rather enhanced the CA secretion evoked by ACh. Collectively, these experimental results suggest that losartan at low concentrations inhibits the CA secretion evoked by cholinergic stimulation (both nicotininc and muscarinic receptors) as well as by membrane depolarization from the rat adrenal medulla, but at high concentration it rather inhibits ACh-evoked CA secretion. It seems that losartan has a dual action, acting as both agonist and antagonist to nicotinic receptors of the rat adrenal medulla, which might be dependent on the concentration. It is also thought that this inhibitory effect of losartan may be mediated by blocking the influx of both $Na^+$ and $Ca^{2+}$ into the rat adrenomedullary chromaffin cells as well as by inhibiting the $Ca^{2+}$ release from the cytoplasmic calcium store, which is thought to be relevant to the $AT_1$ receptor blockade, in addition to its enhancement of the CA release.