• Biomolecules & Therapeutics
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• v.15 no.2
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• pp.108-117
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• 2007

The aim of the present study was to investigate the effect of glibenclamide, a hypoglycemic sulfonylurea, which selectively blocks ATP-sensitive K$^+$ channels, on secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane depolarization from the isolated perfused rat adrenal glands. The perfusion of glibenclamide (1.0 mM) into an adrenal vein for 90 min produced time-dependently enhanced the CA secretory responses evoked by ACh (5.32 mM), high K$^+$ (a direct membrane depolarizer, 56 mM), DMPP (a selective neuronal nicotinic receptor agonist, 100 ${\mu}$M for 2 min), McN-A-343 (a selective muscarinic M1 receptor agonist, 100 ${\mu}$M for 2 min), Bay-K-8644 (an activator of L-type dihydropyridine Ca$^{2+}$ channels, 10 ${\mu}$M for 4 min) and cyclopiazonic acid (an activator of cytoplasmic Ca$^{2+}$-ATPase, 10 ${\mu}$M for 4 min). In adrenal glands simultaneously preloaded with glibenclamide (1.0 mM) and nicorandil (a selective opener of ATP-sensitive K$^+$ channels, 1.0 mM), the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were recovered to the considerable extent of the control release in comparison with that of glibenclamide-treatment only. Taken together, the present study demonstrates that glibenclamide enhances the adrenal CA secretion in response to stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization from the isolated perfused rat adrenal glands. It seems that this facilitatory effect of glibenclamide may be mediated by enhancement of both Ca$^{2+}$ influx and the Ca$^{2+}$ release from intracellular store through the blockade of K$_{ATP}$ channels in the rat adrenomedullary chromaffin cells. These results suggest that glibenclamide-sensitive K$_{ATP}$ channels may play a regulatory role in the rat adrenomedullary CA secretion.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.4
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• pp.227-235
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• 2004

The aim of the present study was to examine the effect of leptin on CA release from the isolated perfused model of the rat adrenal gland, and to establish its mechanism of action. Leptin $(1{\sim}100\;ng/ml)$, when perfused into an adrenal vein of the rat adrenal gland for 60 min, enhanced a dose-dependently the secretory responses of CA evoked by ACh $(5.32{\times}10^{-3}\;M)$, DMPP $(10^{-4}\;M)$ and McN-A-343 $(10^{-4}\;M)$, although it alone has weak effect on CA secretion. However, it did not affect the CA secretion evoked by excess $K^+\;(5.6{\times}10^{-2}\;M)$. Leptin alone produced a weak secretory response of the CA. Moreover, leptin (10 ng/ml) in to an adrenal vein for 60 min also augmented the CA release evoked by BAY-K-8644, an activator of the dihydropyridine L-type $Ca^{2+}$ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}$ ATPase. However, in the presence of U0126 $(1\;{\mu}M)$, an inhibitor of mitogen-activated protein kinase (MAPK), leptin no longer enhanced the CA secretion evoked by ACh and DMPP. Furthermore, in the presence of anti-leptin (10 ng/ml), an antagonist of Ob receptor, leptin (10 ng/ml) also no longer potentiated the CA secretory responses evoked by DMPP and Bay-K-8644. Collectively, these experimental results suggest that leptin enhances the CA secretion from the rat adrenal medulla evoked by cholinergic stimulation (both nicotininc and muscarinic receptors), but does not that by membrane depolarization. It seems that this enhanced effect of leptin may be mediated by activation of U0126-sensitive MAPK through the leptin receptors, which is probably relevant to the activation of the dihydropyridine L-type $Ca^{2+}$ channels located on the rat adrenomedullary chromaffin cells.

• Korean Journal of Veterinary Research
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• v.13 no.1
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• pp.5-12
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• 1973

Seventy two guinea pigs were divided into 3 groups; 24 each of control, unilateral thyro-parathyroidectomized and bilateral thyro-parathyroidectomized groups. After the intraperifoneal in jection of $16{\mu}Ci$ of radioactive calcium ($^{45}Ca$) $^{45}Ca$ uptake of various organs and tissues were measured at the 8th, 16th, 24th and 36th hours, respectively, 18 animals were slaughtered (6 from each group) each time. The results obtained were as follows: 1. It was shown that each organ and tissue of treated animals had higher $^{45}Ca$ uptake than the control group, and the bilateralectomized group, higher than the unilateralectomized group, generally. However, there were some exceptions of the findings. The unilateralectomized group had higher $^{45}Ca$ uptake than the bilateralectomized group in case of adrenal gland and femur at the 8th hour; adrenal gland and blood at the 16th hour; spleen, pancreas, adrenal gland, femur and skeletal muscle at the 24th hour; and pancreas, femur and skeletal muscle at the 36th hour, respectively. 2. $^{45}Ca$ uptakes of each organ and tissue were also determind with respect to time. The results were varied with each treatment group, but generally the highest uptake was shown at the 8th hour and decreased gradually thereafter. The differences were not, however, statistically significant. 3. Femur had shown the highest $^{45}Ca$ uptake and the next were blood, pancreas, liver, skeletal muscle and spleen respectively, and the least were adrenal gland and liver, even though there were some variations in the results. 4. The differences in $^{45}Ca$ uptake of each organ and tissue for the treatment group were statstically significant as compared with the test of the control group, except the spleen and blood at the 8th hour; liver at the 16th hour; adrenal gland, spleen, pancreas at the 24th hour; and spleen at the 36th hour.

• Proceedings of the Ginseng society Conference
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• 1988.08a
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• pp.55-62
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• 1988

The effect of panaxadiol (PD). an active component of Korean ginseng saponins on the secretion of catecholamines (CA) from the rabbit adrenal gland and its mode of action were investigated. PD ($400\;{\mu}g$) increased significantly the secretion of CA from the isolated perfused rabbit adrenal gland. PD-induced secretion of CA was reduced markedly by treatment with atropine. CA secretion induced by Ach or PD was potentiated by physostigmine treatment. Chlorisondamine inhibited CA secretion of PD or Ach. Perfusion of PD ($400\;{\mu}g$) for 30 minutes enhanced the secretory activity of CA by Ach. Ouabain weakened the secretory rsponse caused by PD but enhanced the response by Ach. Adenosine treatment resulted in marked increase in CA secretion by PD or Ach. Perfusion with calcium free Krebs solution containing 5 mM EDTA for 30 minutes completely blocked the secretory effect induced by Ach and also weakened that evoked by PD. It is suggested that PD causes the secretion of CA from the rabbit adrenal gland by a calcium dependent exocytotic process. The secretory effect of PD is due to the stimulation of cholinergic muscarinic and nicotinic-receptors present in the adrenal gland partly by direct action on the chromaffin cell.

• Journal of the Korean Society of Radiology
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• v.84 no.6
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• pp.1408-1413
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• 2023

Adrenal gland trauma is uncommon and is diagnosed at an increasing frequency using CT scans. However, owing to the rarity of this injury and its diverse clinical presentations and prognoses, there is no consensus on its management. In this case report, a 73-year-old male patient experienced recurrent bleeding in the right adrenal gland due to an in-car traffic accident, which was treated with repeated transcatheter arterial embolization.

• The Korean Journal of Pharmacology
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• v.27 no.1
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• pp.53-67
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• 1991

The characteristics and differences between DMPP and McN-A-343 on the secretory effect of catecholamines(CA) were studied in the isolated perfused rat adrenal glands. DMPP(100 uM) and McN-A-343(100 uM) perfused into an adrenal vein of the gland casued significant increases in CA secretion. On molar basis the secretory effect of McN-A-343 was about one fifth as potent as that of DMPP. Tachyphylaxis to releasing effects of CA evoked by DMPP and McN-A-343 was not observed by repeated perfusion of these agents. The DMPP-evoked CA secretion was significantly inhibited by pretreatment with chlorisondamine, desipramine and profusion of $Ca^{2+}-free$ Krebs solution containing EGTA, while it was not affected by pirenzepine, ouabain and physostigmine. However, pretreatment with atropine rather enhanced CA release by DMPP. The releasing effect of CA induced by McN-A-343 was markedly depressed by pretreatment with atropine, pirenzepine, chlorisondamine, physostigmine, and perfusion of $Ca^{2+}-free$ medium plus EGTA but was not influenced by desipramine, except for the case of ouabain which clearly potentiated CA release by McN-A-343. These experimental results suggest that both DMPP and McN-A-343 cause greatly secretion of CA from the isolated perfused rat adrenal glands by a calcium-dependent exocytotic mechanism. The secretory effect of DMPP is due to the stimulation of cholinergic nicotinic receptors and the secretion by McN-A-343 via activation of selecive $M_{1}-muscarinic$ receptors in the adrenal gland. It is also thought that the DMPP-evoked secretory effect is much greater than McN-A-343-induced effect.

• Korean Journal of Animal Reproduction
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• v.4 no.1
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• pp.35-45
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• 1980

The purpose of this experiment was to investigate the effects of castration and administration of testosterone propionate(TP) on the development of the thyroid, adrenal glands and the testis in immature male rats, 25 days immatured, weighing 64.1${\pm}$2g, were divided into two groups of control and castrated, each sub-divided into 30 rats again, treated and untreated with TP respectivity. Each rat was given 20$m\ell$ of TP subcutaneously at two weeks interval. Six rats among each group were randomly sacrificed at 7, 21, 35, 49, and 63 days after treatment, of which their thyroid, adrenal glands and testis were collected for cytometric observation. The results obtained were as follows. 1. The size of the follicle of thyroid glands had a tendency to increase proportionally to the treatment period in every group. However, in castration group, the follicular size of the untreated with TP were significantly increased from 49 days (p<0.05) after treatment than that of the treated with TP, while in control group, the treated with TP were not increased during the treatment period. Regarding the height of the follicular epithelial cell in thyroid gland, the treated with TP had a tendency to increase than the untreated with TP in both castration and control group. 2. Regarding the size of the follicle of thyroid gland in relation with the increment period, the untreated with TP in control group were slightly increased from 49 days after treatment, but the treated with TP were not changed significantly. Castration group had a tendency to increase significantly than the control group, especially the untreated with TP in castration group were significantly increased. 3. As for the change of the relative height of thyroidal follicular epithelial cell in relation with the increment of treatment period, the untreated, A and C group, in both castration and control group were increased at 35 days 63 days after treatment while the treated, B and D group had tendency to increase from 21 days after treatment. 4. Regarding the thickness fo adrenal cortex, the castration group had a tendency to increase than the control group until 21 days after treatment. But, at 35 days, the change of the thickness was reversed; Mean while at 49 days and 63 days, especially C group in castration were significantly increased than any other groups although there were no significant differences among the every group during the whole treatment period. Regarding the thickness of adrenal cortex in relation with the increment of treatment period, A, B and C group had a tendency to increase until 21 days after treatment. After that period, there was no significant increment in all groups. Especially, in D group, there were no significant changes from 7 days to 63 days after treatment. 5. As for the tickness of adrenal medulla, there were no significant changes in every group of castration and TP treatment, except that the castration group had a tendency to increase continually than the control throughout the whole treament period. 6. In terms of the number, diameter and thickness of seminiferous tubule in testis of control group, the treated group with TP were distinctly reduced than those of the untreated group from 49 days after treatment respectively.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.83.2-83.2
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• 2003

It has been demonstrated the presence of leptin receptors (Ob-Ra) on epinephrine-secreting chromaffin cells in rat adrenal medulla, suggesting that leptin may directly affect the adrenal medulla (Cao et al., 1997). Leptin is found to stimulate catecholamine (CA) synthesis in cultured bovine adrenal medullary cells (Utsumomiya et al., 2001; Shibuya et al., 2002)and cultured porcine adrenal medullary cells (Takekoshi et al., 2001). Thus, the present study was designed to examine the effect of leptin on CA release from the isolated perfused rat adrenal gland, and to establish its mechanism of action. (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.5
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• pp.265-272
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• 2004

The present study was attempted to investigate the effect of cilnidipine (FRC-8635), which is a newly synthesised novel dihydropyridine (DHP) type of organic $Ca^{2+}$ channel blockers, on secretion of catecholamines (CA) evoked by acetylcholine (ACh), high $K^+$, DMPP and McN-A-343 from the isolated perfused rat adrenal gland. Cilnidipine $(1{\sim}10{\mu}M)$ perfused into an adrenal vein for 60 min produced relatively dose- and time-dependent inhibition in CA secretory responses evoked by ACh $(5.32{\times}10^{-3}M),\;DMPP\;(10^{-4}M\;for\;2\;min)$ and McN-A-343 $(10^{-4}M\;for\;2\;min)$. However, lower dose of cilnidipine did not affect CA secretion by high $K^+\;(5.6{\times}10^{-2}\;M)$, higher dose of it reduced greatly CA secretion of high $K^{+}$. Cilnidipine itself did fail to affect basal catecholamine output. In the presence of cilnidipine $(10{\mu}M)$, the CA secretory responses evoked by Bay-K-8644 $(10{\mu}M)$, an activator of L-type $Ca^{2+}$ channels and cyclopiazonic acid $(10{\mu}M)$, an inhibitor of cytoplasmic $Ca^{2+}$-ATPase were also inhibited. Moreover, ${\omega}-conotoxin\;GVIA\;(1{\mu}M)$, a selective blocker of the N-type $Ca^{2+}$ channels, given into the adrenal gland for 60 min, also inhibited time-dependently CA secretory responses evoked by Ach, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid. Taken together, these results demostrate that cilnidipine inhibits CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors from the isolated perfused rat adrenal gland without affecting the basal release. However, at lower dose, cilnidipine did not affect CA release by membrane depolarization while at larger dose inhibited that. It seems likely that this inhibitory effect of cilnidipine is exerted by blocking both L- and N-type voltage-dependent $Ca^{2+}$ channels (VDCCs) on the rat adrenomedullary chromaffin cells, which is relevant to inhibition of both the $Ca^{2+}$ influx into the adrenal chromaffin cells and intracellular $Ca^{2+}$ release from the cytoplasmic store. It is thought that N-type VDCCs may play an important role in regulation of CA release from the rat adrenal medulla.

• Korean Journal of Animal Reproduction
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• v.4 no.1
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• pp.47-74
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• 1980

The present experiments were carried out to elucidate the effects of hypophysectomy and subsequent administration of sex hormone on thyroid, adrenal gland, gonads and blood plasma components in the rat. The jresults obtained were summarized as follows: The weight of the thyroid gland of both male and female hypophysectiomzed rats decreased markedly from 7 days up to 56 days after the hypophysectomy as compared to the control group. The administration of sex hormone (6 mg of testosterone propionate to male and 6 mg of hexestrol to female) to the hypophysectomized rat gave on effect on the change in the weight of the thyroid gland. The hopophysectomy decreased the uptake of radioactive iodine in the thyroid gland in both male and female rats with time. Subsequent administration of the sex hormone caused no effect. With regard to the histological changes of the thyroid gland, the hypophysectomy caused significant changes in the gland showing a remarkable degeneration. The function of the gland seemed to disa, pp.ar almost completely on 56th day after the hypophysectomy. Upon the administration of sex hormone after the hypophysectomy, however. the epithelia of the follicle which has changed to flat from has partly returned to its functional cubicfrom and nuclei recovered as nearly as normal. These recovery were more remarkable in the female than in the male. The hypophysectomy kept causing a significant decrease in the weight of the adrenal gland in male and female rats during the period of observation (up to 56 days) as in the case of thyroid gland. The administration of sex hormone has on effect in this respect either. The hypophysectomy also caused a marked morphological change in the gland: zona fasciculata and zona reticularis were dicreased in size quichly after the hypophysectomy. The administraton of the sex hormone to the hypophysectomized rat resulted in clear distinction among the three layers of the adrenal cortex which otherwise very diffused. In the male, this phenomenum was more remarkable than in the female and the pattern of the cell arrangements and the thickening of each layer became similar to those of normal rats. The gonads of both sexes have also kept decreasing in the weight and degenerated in morpohology after the hypophysectomy. However, the degenerate follicle became enlarged after the administration of hexestrol in the female. Furthermore, the vacuoles found in interstitial cells of hypophysectomized rat disa, pp.ared after the administration of testosterone in the male and the formation of spermatocytes seemed to be recovered. Hypophysectomy also caused a gradual increase in the contents of total protein, non-protein nitrogen, total lipid, cholesterol and calcium in the blood plasma with time. The concentrations of sodium, potassium and chloride in the blood did not change after the hypophysectomy. Sex hormone caused practically no change in above tendency.