• Applied Microscopy
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• v.33 no.4
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• pp.291-298
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• 2003

Exposure to stressful stimuli is known to activate the peripheral sympathetic nervous system and the adrenal gland. In this study, we evaluated the effects of high-salt diet on the mouse adrenal medulla using the tyrosine hydroxylase (TH) immunohistochemistry and the transmission electron microscopic observation. Immunoreactivity for TH was increased after high-salt diet. Especially, the TH immunoreactivity was stronger in 4 days high-salt diet mouse than that of 4 weeks. TH immunoreactivity was mainly present in the cytoplasm and granules of the noradrenaline cells. After high-salt diet, the noradrenaline cells exhibited the ultrastructural alterations consisting of areas of empty cytoplasm, expanded granules, and some damaged mitochondria. These results suggest that high-salt diet may be a factor of stressful stimuli on the mouse.

• Biomolecules & Therapeutics
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• v.12 no.3
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• pp.165-174
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• 2004

The aim of the present study was to investigate the effect of FCCP (carbonyl cyanide p-trifluoromethoxyphenyIhydrazone), which is a potent mitochondrial uncoupler, on secretion of catecholamines (CA) from the perfused model of the rat adrenal gland and to establish the mechanism of its action. The perfusion of FCCP (3 ${\times}$ $10^{-5}$ M) into an adrenal vein of for 90 min resulted in great increases in CA secretions. Tachyphylaxis to CA-releasing effect of FCCP was not observed by repeated perfusion of it. The CA-releasing effects of FCCP were depressed by pre-treatment with pirenzepine, chlorisondamine, nicardipine, TMB-8, and the perfusion of EGTA plus $Ca^{2+}$-free medium. In the presence of FCCP (3 ${\times}$ $10^{-5}$ M), the CA secretory responses induced by Ach (5.32 ${\times}$ $10^{-3}$ M), and DMPP ($10^{-4}$ M) were significantly enhanced. Furthermore, the perfusion of CCCP (3 ${\times}$ $10^{-5}$ M), a similar mitochondrial uncoupler, into an adrenal vein for 90 min also caused an increased response in CA secretion. Taken together these experimental results indicate that FCCP causes the CA secretion the perfused rat adrenal medulla in a calcium-dependent fashion. It is suggested that this facilitatory effects of FCCP may be mediated by cholinergic receptor stimulation, which is relevant to both stimulation of the $Ca^{2+}$ influx and $Ca^{2+}$ release from cytoplasmic $Ca^{2+}$ stores.

• Biomolecules & Therapeutics
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• v.17 no.1
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• pp.32-42
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• 2009

The purpose of the present study was to examine the effect of dihydrexidine, a full $D_1$ receptor agonist, on the secretion of catecholamines (CA) from the perfused model of the rat adrenal gland, and to establish its mechanism of action. Dihydrexidine (10-100 ${\mu}M$), perfused into an adrenal vein for 60 min, relatively produced dose- and time-dependent inhibition in the CA secretory responses evoked by ACh (5.32 mM), high $K^+$ (56 mM), DMPP (100 ${\mu}M$) and McN-A-343 (100 ${\mu}M$). Dihydrexidine itself did fail to affect basal CA output. Also, in adrenal glands loaded with dihydrexidine (30 ${\mu}M$), 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, and veratridine, an activator of voltage-dependent $Na+$ channels (10 ${\mu}M$), were also markedly inhibited, respectively. However, in the simultaneous presence of dihydrexidine (30 ${\mu}M$) and R (+)-SCH23390 (a selective antagonist of $D_1$ receptor, 3 ${\mu}M$), the CA secretory responses evoked by ACh, high K+, DMPP, McN-A-343, Bay-K-8644, cyclopiazonic acid and veratridine were considerably recovered to the extent of the corresponding control secretion compared with the inhibitory responses by dihydrexidinetreatment alone. In conclusion, these experimental results suggest that dihydrexidine significantly inhibits the CA secretion evoked by cholinergic stimulation (both nicotinic and muscarinic receptors) and membrane depolarization from the rat adrenal medulla. It seems that this inhibitory effect of dihydrexidine may be mediated by inhibiting influx of both $Ca^{2+}$ and $Na^+$ into the cytoplasm as well as by suppression of $Ca^{2+}$ release from cytoplasmic calcium store through activation of dopaminergic $D_1$ receptors located on the rat adrenomedullary chromaffin cells.

• Korean Journal of Veterinary Research
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• v.37 no.3
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• pp.463-469
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• 1997

This study was performed to investigate the gross anatomical features and microscopical structures of the hemal nodes and the hemolymph nodes in the water deer (Hydropotes inermis) found in Kangwon-do, Korea. The hemal nodes and hemolymph nodes were observed mainly in the periphery of the thoracic and abdominal aortae of the animals. The size of hemal nodes was generally smaller than that of the hemolymph nodes, and the shape of the both organs was spherical or ovoid. The color of the hemal nodes was red or black while that of the hemolymph nodes was gray with red bands. The hemal nodes were surrounded by a thin connective tissue capsule and there were extensive subcapsular and deep sinuses distended by a great number of erythrocytes. Although a few number of lymphatic nodules and small areas of diffuse lymphatic tissues were observed in the parenchyma, no typical cortex and medulla were defined in the hemal node. Small numbers of blood vessels were found at the connective tissue capsule but lymph vessel was not observed microscopically in this organ. The hemolymph nodes were covered by a relatively thick connective tissue capsule and there was a hilus in each node. The parenchyma was divided into cortex and medulla. The cortex was composed of a few numbers of lymphatic nodules and some diffuse lymphatic tissues. The medulla comprised medullary sinus and cords. Afferent and efferent lymph vessels were observed at the periphery of the capsule and the hilus, respectively. The subcapsular and medullary sinuses were not extensive but filled with small numbers of erythrocytes. The stroma of hemal node and hemolymph node was composed of reticular cells and fibers, and the capsule and trabecula consisted of collagenous fibers with smooth muscle fibers.

• 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.

• 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.

• International Journal of Stem Cells
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• v.16 no.2
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• pp.168-179
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• 2023

Background and Objectives: We evaluated the effect of adipose-derived stem cell-derived conditioned medium (ADSC-CM) on the renal function of rats with renal ischemia-reperfusion injury (IRI)-induced acute kidney injury. Methods and Results: Forty male Sprague-Dawley rats were randomly divided into four groups: sham, nephrectomy control, IRI control, ADSC-CM. The ADSC-CM was prepared using the three-dimensional spheroid culture system and injected into renal parenchyme. The renal function of the rats was evaluated 28 days before and 1, 2, 3, 4, 7, and 14 days after surgical procedures. The rats were sacrificed 14 days after surgical procedures, and kidney tissues were collected for histological examination. The renal parenchymal injection of ADSC-CM significantly reduced the serum blood urea nitrogen and creatinine levels compared with the IRI control group on days 1, 2, 3, and 4 after IRI. The renal parenchymal injection of ADSC-CM significantly increased the level of creatinine clearance compared with the IRI control group 1 day after IRI. Collagen content was significantly lower in the ADSC-CM group than in the IRI control group in the cortex and medulla. Apoptosis was significantly decreased, and proliferation was significantly increased in the ADSC-CM group compared to the IRI control group in the cortex and medulla. The expressions of anti-oxidative makers were higher in the ADSC-CM group than in the IRI control group in the cortex and medulla. Conclusions: The renal function was effectively rescued through the renal parenchymal injection of ADSC-CM prepared using a three-dimensional spheroid culture system.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.38 no.3
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• pp.275-282
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• 2012

In this study, the antioxidative effects of extracts from different parts of Juncus effusus L. were investigated. The three parts (above-ground part, below-ground part, medulla part) were selected. 50 % ethanol extract, ethyl acetate and aglycone fractions of J. effusus L. were used in experiments. The highest DPPH (1,1-diphenyl-2-picrylhydrazyl) scavenging activities ($FSC_{50}$) was shown by medulla part (42.9 ${\mu}g/mL$) in 50 % ethanol extracts, below-ground part (12.1 ${\mu}g/mL$) in ethyl acetate fractions, and below-ground part (12.1 ${\mu}g/mL$) in aglycone fractions. Reactive oxygen species (ROS) scavenging activities ($OSC_{50}$) on ROS generated in $Fe^{3+}$-EDTA/$H_2O_2$ system using the luminol-dependent chemiluminescence assay showed the most prominent effect of medulla part (0.29 ${\mu}g/mL$) in 50 % ethanol extracts, below-ground part (0.25 ${\mu}g/mL$) in ethyl acetate fractions, and medulla part (0.20 ${\mu}g/mL$) in aglycone fractions. The cellular protective effects of extract/fractions of J. effusus L. on the rose-bengal sensitized photohemolysis of human erythrocytes were increased in a concentration dependent manner (0.5 ~ 10 ${\mu}g/mL$). Especially, aglycone fraction of medulla part at a concentration of 10 ${\mu}g/mL$ showed the most prominent protective effect among all extracts (${\tau}_{50}$, 321.0 min). These results indicate that extracts from below-ground part and medulla part of J. effusus L. extracts can be used as an natural antioxidant. Particularly, J. effusus L. can protect suggesting a high ${\tau}_{50}$ skin where many $^1O_2$ was generated by sunlight exposure.

• Applied Microscopy
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• v.37 no.4
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• pp.271-280
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• 2007

Tonicity-responsive enhancer binding protein(TonEBP) is a transcriptional factor essential in the function and development of the renal medulla. TonEBP plays a critical role in protecting renal medullary cells from the deleterious effect of hypertonicity. TonEBP is a key regulator of urinary concentration via stimulation of transcription of urea transporter(UT) in a manner independent of vasopressin. UT in the renal inner medulla is important for the conservation of body water due to its role in the urine concentrating mechanism. Mongolian gerbil(Meriones unguiculatus) has been as an model animal for studying the neurological disease such as stroke and epilepsy because of the congenital incomplete in Willis circle, as well as the investigation of water metabolism because of the long time-survival in the condition of water-deprived desert condition, compared with other species animal. In this study, we divide 3 groups of which each group include the 5 animals. In the study of 7 or 14 days water restricted condition, we investigated the TonEBP and UT-A by using a immunohistochemistry in the kidney. In the normal kidney, the distribution of TonEBP is generally localized on nuclei of inner medullary cells. Nuclear distribution of TonEBP is generally increased throughout the medulla in 7 and 14 days dehydrated group compared with control group. Increased nuclear localization was particularly dramatic in thin limbs. In control groups, UT-A was expressed in inner stripe of outer medulla(ISOM) and inner medulla(IM). UT-A was present in the terminal part of the short-loop of descending thin limbs (DTL) in ISOM and also present in the inner medullary collecting duct(IMCD), where the intensity of it gradually increased toward the papillary tip. In the dehydrated kidney, UT-A immunoreactivity was increased in the short-loop of DTL in ISOM and in the long-loop of DTL in the initial part of IM, where was expressed moderate positive reaction in the normal kidney. Also it was up regulated in the IMCD in initial & middle part of IM. However UT-A down regulated in the IMCD, where the intensity of it gradually decreased toward the papillary tip. These findings suggest that increased levels of TonEBP in medulla and UT-A in shot-loop of DTL and IMCD play a important role for maintain fluid balance in the water-deprived mongolian gerbil kidney.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.5
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• pp.431-439
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• 2014

The aim of the present study was to investigate whether ginsenoside-Rb2 (Rb2) can affect the secretion of catecholamines (CA) in the perfused model of the rat adrenal medulla. Rb2 ($3{\sim}30{\mu}M$), perfused into an adrenal vein for 90 min, inhibited ACh (5.32 mM)-evoked CA secretory response in a dose- and time-dependent fashion. Rb2 ($10{\mu}M$) also time-dependently inhibited the CA secretion evoked by DMPP ($100{\mu}M$, a selective neuronal nicotinic receptor agonist) and high $K^+$ (56 mM, a direct membrane depolarizer). Rb2 itself did not affect basal CA secretion (data not shown). Also, in the presence of Rb2 ($50{\mu}g/mL$), the secretory responses of CA evoked by veratridine (a selective $Na^+$ channel activator ($50{\mu}M$), Bay-K-8644 (an L-type dihydropyridine $Ca^{2+}$ channel activator, $10{\mu}M$), and cyclopiazonic acid (a cytoplasmic $Ca^{2+}$-ATPase inhibitor, $10{\mu}M$) were significantly reduced, respectively. Interestingly, in the simultaneous presence of Rb2 ($10{\mu}M$) and L-NAME (an inhibitor of NO synthase, $30{\mu}M$), the inhibitory responses of Rb2 on ACh-evoked CA secretory response was considerably recovered to the extent of the corresponding control secretion compared with the inhibitory effect of Rb2-treatment alone. Practically, the level of NO released from adrenal medulla after the treatment of Rb2 ($10{\mu}M$) was greatly elevated compared to the corresponding basal released level. Collectively, these results demonstrate that Rb2 inhibits the CA secretory responses evoked by nicotinic stimulation as well as by direct membrane-depolarization from the isolated perfused rat adrenal medulla. It seems that this inhibitory effect of Rb2 is mediated by inhibiting both the influx of $Ca^{2+}$ and $Na^+$ into the adrenomedullary chromaffin cells and also by suppressing the release of $Ca^{2+}$ from the cytoplasmic calcium store, at least partly through the increased NO production due to the activation of nitric oxide synthase, which is relevant to neuronal nicotinic receptor blockade.