• Applied Microscopy
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• v.28 no.2
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• pp.215-224
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• 1998

To investigate ultrastructural changes on the adrenal glands of the developmental rats, tissues were collected at 20 days of gestation, at birth, 7 days, 15 days and 30 days after birth and studied by electron microscope. In the medulla of adrenal gland of the rat, two types of granules were observed at ultrastructural level. The one were adrenaline $(123\sim200nm)$ and the others were noradrenaline ($177\sim279nm$ of long axis, $124\sim194$ of short axis). Adrenaline granules were characterized by presence of round or spherical with low or moderate electron density. The granules showed a wide lucent or clean halo between the contents and the limiting membrane. On the other hand noradrenaline granules were characterized by the presence of irregular shape with high electron density. This granules showed a wide lucent between the contents and limiting membrane. These two types of granules were co-existed in one cell in the late gestation and at birth, but after that two types of cells were clearly observed. The different sizes and numbers of granules were observed with ages.

• The Korean Journal of Pharmacology
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• v.3 no.1
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• pp.5-13
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• 1967

It has been reported by some investigators that pressor response of rabbits to sympathetic ganglionic stimulants was weak. In this paper it was attempted to investigate this problem more thorouglhy in urethane anesthetized rabbits. 1) In rabbits the approximate doses to elicit increase of about 20 mmHg of blood pressure were $100\;{\mu}g/kg$ with DMPP, $50\;{\mu}g/kg$ with Wy-615, $500\;{\mu}g/kg$ with TMA and with nicotine. The pressor activity of these substances was markedly augmented by treating animals with syrosingopine. 2) In adrenal-ligated rabbits pressor activity of the substances was markedly reduced. Treating the adrenal-ligated animals with syrosingopine augmented significantly the pressor activity of these substances except DMPP. Direct injection of DMPP and TMA into the adrenal produced mole pressor response than intravenous injection did. These date suggest that DMPP has greater effect on the adrenal medulla than the other substances. 3) In vagotomized and atropinized rabbits the pressor activity of these compounds was more marked than in normal rabbits. 4) The above facts indicate that the pressor activity of the ganglionic stimulants in rabbits was definitely low than in cats and dogs. The low responsiveness of the rabbits to these agents was discussed in the light of catecholamine releasing mechanisms, and extraganglionic actions of these substances.

• Biomolecules & Therapeutics
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• v.10 no.3
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• pp.142-151
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• 2002

The present study was attempted to investigate the effect of apamin on catecholamine (CA) secretion evoked by ACh, high $K^+$, DMPP, McN-A-343, cyclopiazonic acid and Bay-K-8644 from the isolated perfused rat adrenal gland and to establish the mechanism of its action. The perfusion of apamin (1 nM) into an adrenal vein for 20 min produced greatly potentiation in CA secretion evoked by ACh (5.32 $ imes$ $10^{-3}$ M), high $K^+$, (5.6 $ imes$ $10^{-2}$), 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). However, apamin itself did fail to affect basal catecholamine output. Furthermore, in adrenal glands preloaded with apamin (1 nM) under the presence of glibenclamide ($10^{-6}$ M), an antidiabetic sulfonylurea that has been shown to be a specific blocker of ATP-regulated potassium channels (for 20 min), CA secretion evoked by DMPP and McN-A-343 was not affected. However, the perfusion of high concentration of apamin (100 nM) into an adrenal vein for 20 min rather inhibited significantly CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, cyclopiazonic acid and Bay-K-8644. Taken together, these results suggest that the low concentration of apamin causes greatly the enhancement of CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization. These findings suggests that apamin-sensitive SK ($Ca^{2+}$) channels located in rat adrenal medullary chromaffin cells may play an inhibitory role in the release of catecholamines mediated by stimulation of cholinergic nicotinic and muscarinic receptors as well as membrane depolarization. However, it is thought that high concentration of apamin cause the inhibitory responses in catecholamine secretion evoked by stimulation of cholinergic receptors as well as by membrane depolarization from the rat adrenal gland without relevance with the SK channel blockade.

• The Korean Journal of Physiology and Pharmacology
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• v.12 no.1
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• pp.13-23
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• 2008

The aim of the present study was designed to establish comparatively the inhibitory effects of $D_1$-like and $D_2$-like dopaminergic receptor agonists, SKF81297 and R(-)-TNPA on the release of catecholamines (CA) evoked by cholinergic stimulation and membrane depolarization from the isolated perfused model of the rat adrenal medulla. SKF81297 $(30{\mu}M)$ and R-(-)-TNPA $(30{\mu}M)$ perfused into an adrenal vein for 60 min, produced great inhibition in the CA secretory responses evoked by ACh $(5.32{\times}10^{-3}\;M)$, DMPP $(10^{-4}\;M)$, McN-A-343 $(10^{-4}\;M)$, high $K^+$ $(5.6{\times}10^{-2}\;M)$, Bay-K-8644 $(10{\mu}M)$, and cyclopiazonic acid $(10{\mu}M)$, respectively. For the release of CA evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid, the following rank order of inhibitory potency was obtained: SKF81297>R-(-)-TNPA. However, R(+)-SCH23390, a selectve $D_1$-like dopaminergic receptor antagonist, and S(-)-raclopride, a selectve $D_2$-like dopaminergic receptor antagonist, enhanced the CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid only for $0{\sim}4$ min. The rank order for the enhancement of CA release evoked by high $K^+$, McN-A-343 and cyclopiazonic acid was R(+)-SCH23390>S(-)-raclopride. Also, the rank order for ACh, DMPP and Bay-K-8644 was S(-)-raclopride > R(+)-SCH23390. Taken together, these results demonstrate that both SKF81297 and R-(-)-TNPA inhibit the CA release evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors and the membrane depolarization from the isolated perfused rat adrenal gland without affecting the basal release, respectively, but both R(+)-SCH23390 and S(-)-raclopride facilitate the CA release evoked by them. It seems likely that the inhibitory effects of SKF81297 and R-(-)-TNPA are mediated by the activation of $D_1$-like and $D_2$-like dopaminergic receptors located on the rat adrenomedullary chromaffin cells, respectively, whereas the facilitatory effects of R(+)-SCH23390 and S(-)-raclopride are mediated by the blockade of $D_1$-like and $D_2$-like dopaminergic receptors, respectively: this action is possibly associated with extra- and intracellular calcium mobilization. Based on these results, it is thought that the presence of dopaminergic $D_1$ receptors may play an important role in regulation of the rat adrenomedullary CA secretion, in addition to well-known dopaminergic $D_2$ receptors.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.4
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• pp.223-230
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• 2005

The purpose of the present study was to examine the effect of naltrexone, an opioid antagonist, on secretion of catecholamines (CA) evoked by cholinergic nicotinic stimulation and membrane-depolarization from the isolated perfused rat adrenal gland and to establish the mechanism of its action. Naltrexone $(3{\times}10^{-6}M)$ perfused into an adrenal vein for 60 min produced time-dependent inhibition in CA secretory responses evoked by ACh $(5.32{\times}10^{-3}M)$ , high $K^+$ $(5.6{\times}10^{-2}M)$ , DMPP ($10^{-4}$ M) and McN-A-343 $(10^{-4}M)$ . Naltrexone itself did also fail to affect basal CA output. In adrenal glands loaded with naltrexone $(3{\times}10^{-6}M)$ , 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. However, in the presence of met-enkephalin $(5{\times}10^{-6}M)$ , 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. Collectively, these experimental results demonstrate that naltrexone inhibits greatly CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that this inhibitory effect of naltrexone 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.

• Development and Reproduction
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• v.2 no.1
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• pp.39-43
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• 1998

The synthesis of steroid hormone starts from cholesterol. Steroidogenic acute regulatory protein(StAR) transfers cholesterol acutely from the outer mitochondrial membranes to the inner in the early step of steroidogenesis. Many kinds of steroid hormones are mainly synthesized in adrenal grand, ovary and testis. The purpose of this study is to determine the distribution of StAR mRNA in the rat ovary and adrenal gland and to confirm the functions of StAR in these organs. In the ovary, StAR mRNAs were strongly expressed in the corpus luteum, where progesterone is synthesized, and these were weakly expressed in the theca layer of follicles, where androgen is synthesized. However, StAR mRNAs were not detected in the estrogen producing granulosa cells of growing follicles. In the corpus luteum, StAR mRNAs were strongly loclized in the zona fasciculata and zona reticularis, where glucocorticoid is mainly synthesized. StAR mRNAs were weakly expressed in the zona gromerulosa, where mineralcorticoid is synthesized. StAR mRNAs were not detected in the adrenal medulla. In our results, StAR mRNAs were expressed differentially in the steroidogenic cells of ovary and adrenal gland according to the types of steroid hormones, and the statges of corpus luteum development. We conclude that StAR is involved in the steroidogenesis at the very early step of steroid synthesis cascade.

• The Korean Journal of Pharmacology
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• v.30 no.3
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• pp.299-311
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• 1994

The present study was attempted to investigate whether pentazocine, which is known to possess both opioid agonistic and antagonistic properties, produces catecholamines (CA) secretion from the isolated perfused rat adrenal gland, and to establish the mechanism of its action, and also to compare its action with that of some opioids. Pentazocine (30 to 300 ug) injected into an adrenal vein caused a dose-dependent secretory response of CA from the rat adrenal medulla. The pentazocine-evoked secretion of CA was remarkably diminished by the preloading with chlorisondamine $(10^{-6}\;M)$, naloxone $(1.22{\times}10^{-7}\;M)$, morphine $(1.7{\times}10^{-5}\;M)$, met-enkephalin $(9.68{\times}10^{-6}\;M)$, nicardipine $(10^{-6}\;M)$ and TMB-8 $(10^{-5}\;M)$ while was not influenced by the pretreatment of pirenzepine $(2{\times}10^{-6}\;M)$. The perfusion of $Ca^{++}$-free Krebs solution for 30 min into the gland also led to the marked reduction in CA secretion evoked by pentazocine. Furthermore, the CA release evoked by ACh and/or DMPP was greatly inhibited by the pretreatment with pentazocine $(1.75{\times}10^{-4}\;M)$ for 20 min. From these experimental results, it is thought that pentazocine causes markedly the increased secretion of CA from the isolated perfused rat adrenal medulla by a calcium-dependent exocytotic mechanism. The secretory effect of pentazocine appears to be mediated through activation of opioid receptors located on adrenal chromaffin cells, which may be also associated with stimulation of cholinergic nicotinic receptors.

• Toxicological Research
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• v.9 no.2
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• pp.187-194
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• 1993

[Met5]-Enkephalin (ME) secretion and the expression of proenkephalin A (proENK) mRNA were studied following long-term exposure of bovine adrenal medullary chromaffin (BAMC) cells to pertussis toxin. Prolonged (24 hr) stimulation of BAMC cells with pertussis toxin increased the secretion of ME as well as proENK gene expression. BAMC cells were also incubated with pertussis toxin in the presence or absence of other secretagogues such as nicotine, angiotensin II and phorbol myristate acetate.

• Korean Journal of Veterinary Research
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• v.15 no.1
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• pp.39-45
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• 1975

The authors believe that farm livestok will be greatly affected by the marked increasing use of organic phosphate. This study was carried out to observe the clinical signs and histopathological changes of mouse, guinea pig, hamster and rabbit that were orally administered with diazinon used usually as agricultural insecticide, and cholinesterase (ChE) activity was histochemically examined in the liver, heart, kidney, adrenal gland, duodenum and salivary gland of these experimental animals administered with diazinon. The results obtained were as follows: 1. Clinical signs such as dullness, severe salivation, ataxia, dyspnea, irregular slight convulsion and inappetance and as the histopathological changes cloudy swelling, congestion and hemorrhage of parenchymal organs, catarrh or local necrsois of the gastrointestinal tract, congestion or hemorrhage of the other organs were observed. Especially, hemorrhage of adrenal glands (rabbit, guinea pig) and pulmonary congestion and hemorrhage were necessarily constant. 2. In the histochemical study, ChE activity appeared intensely in the liver, heart, medulla of adrenal glands and salivary glands (submaxillary and parotid) of control animals, but ChE activity was negative or markedly decreased in experimental animals administered with diazinon. There was no marked difference between the control and experimental animals in ChE activity of the kidney. 3. Histochemical observation of ChE activity was helpful to explain the clinical signs and histopathological changes and was regarded as a diagnostic method for organic phosphate poisoning.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.1
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• pp.141-141
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• 2017