• The Korean Journal of Pharmacology
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• v.32 no.1
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• pp.83-91
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• 1996

The present study was designed to determine the effect of hydrocortisone on CA secretion evoked by histamine from the isolated perfused rat adrenal glands. Histamine (150 ug) given into an adrenal vein produced significantly CA secretion from the rat adrenal medulla. This histamine-evoked CA secretion was enhanced markedly by the pretreatment with the natural glucocorticoid hydrocortisone (30 uM) or the synthetic glucocorticoid dexamethasone 30 (uM) for 20 min, respectively. Hydrocortisone-induced potentiation of CA secretion evoked by histamine was inhibited by preloading with heparin (3.56 U/ml), an $IP_3$ receptor antagonist while more enhanced by forskolin (0.2 uM), a potent stimulator of adenylate cyclase. From the experiment result taken together, it is thought that hydrocortisone (glucocorticoids) can enhance the releasing effect of CA evoked by histamine from the isolated perfused rat adrenal medulla, which seems to be associated to accumulation of inositol phosphate as well as cyclic AMP in the rat adrenomedullary chromaffin cells.

• Journal of the Korean Society of Radiology
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• v.81 no.4
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• pp.912-919
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• 2020

Purpose This study aimed to compare the brain perfusion status of patients with chronic kidney disease to a normal control group to identify any significant differences. Materials and Methods The perfusion state of the brain was measured by MRI using the arterial spin labeling technique in 36 patients undergoing hemodialysis due to chronic kidney disease and 36 normal controls. Images were then analyzed in a voxel-wise manner to detect brain areas showing significant perfusion differences between the two groups. Results Patients with chronic kidney disease showed increased perfusion in the form of large clusters across the right fronto-parieto-temporal lobe and the left parieto-occipital lobe. In addition, perfusion increased in the bilateral thalami, midbrain, pons, and cerebellum (p < 0.01, familywise error corrected). Conclusion Brain perfusion appears to increase in patients with chronic kidney disease compared to normal controls. Uremic toxicity is thought to be the cause of this increase as it can cause damage to the microscopic blood vessels and their surrounding structures.

• The Korean Journal of Pharmacology
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• v.32 no.3
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• pp.357-371
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• 1996

Lithium (Li) is known to be used not only during acute manic psychosis but also acute depressive phase in manic-depression. In the present study, it was attempted to investigate the effect of lithium on catecholamine (CA) secretion from the isolated perfused rat adrenal gland and to clarify the mechanism of its action. Replacement of $Na^+$ (118.4 mM) by lithium in the normal Krebs-bicarbonate solution used to perfuse the gland produced gradually an increased response in the spontaneous catecholamine release, which was peaked at $30{\sim}60$ min after its perfusion. Li-Krebs solution was perfused into an adrenal vein for 2 hours in every experiments. Li-Krebs-evoked CA secretory responses were depressed significantly under loading with $Ca^{++}-free$ medium. This CA secretion evoked by lithium loading was also reduced markedly by the pretreatment with nicardipine ($10^{-6}$ M), TMB-8 ($10^{-5}$ M) and chlorisondamine ($10^{-6}$ M) for 20 min, respectively, while was not affected by preloading with a pirenzepine ($2{\times}10^{-6}$ M)-containing Krebs. $Na^+$ pump inhibition by pretreatment with ouabain ($10^{-4}$ M) for 20 min did make the marked depression in Li-evoked CA secretory responses. Moreover, Li-evoked CA release was also diminished markedly by preloading with tetrodotoxin ($5{\times}10^{-7}$ M)-contaming Krebs for 20 min. All these experimental results taken together suggest that lithium enhances CA secretion in a $Ca^{++}$-dependent fashion by its accumulation in the adrenomedullary chromaffin cells of the rat, and that this secretory effect may be meidated by a dual mechanism: (i) chromaffin cell depolarization and subsequent opening of voltage-sensitive $Ca^{++}$ channels and (ii) activation of a $[Li]_i-[Ca]_0$ counter-transport system.