• Journal of Food Hygiene and Safety
• /
• v.13 no.3
• /
• pp.258-267
• /
• 1998

The acetaminophen (AP AP), an antipyretic and analgesic agent, induces the hepatotoxicity by increasing influx of calcium and destabilizing the cellular membrane which can be caused by N-acetyl-p-benzoquinoneimine generated by cytochrome P-450 (CYF-450) when it is overdosed. Diltiazem (DIL), a calcium channel blocking agent, has been known to suppress the CYF-450 activities. To study the effect of DIL in APAP treated rats, the serum biotransformational enzyme analyses and the liver histopathologic examination were conducted on the rats which had been administered DIL at 3, 6, 9 and 12 hours after the 3,000 mg/kg of APAP administration. Following a single dose of DIL administered 12 hours after AP AP administration, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, malondialdehyde and calcium contents of liver and microsome were significantly reduced. Glutathione S-transferase (GST) activity was significantly increased. Histopathologic studies showed that DIL had prevented the development of centrilobular necrosis induced by AP AP in liver tissue. Our results suggested that diltiazem could inhibit the formation of free radical and the influx of calcium and could increase GST activity. Therefore, diltiazem can be administered at the time of 12 hours after overdosed AP AP to diminish the liver damage.

• Bulletin of the Korean Chemical Society
• /
• v.31 no.9
• /
• pp.2451-2452
• /
• 2010

• Journal of the Korean Society of Food Science and Nutrition
• /
• v.27 no.2
• /
• pp.333-337
• /
• 1998

This study was carried out to get infomation on the nitric oxide production ability and its formation mechanisms of polysaccharides extracted from Ganoderma lucidum(PSG) by using murine macrophage cell line. The cultured mycelial cells of Ganoderma lucidum were extracted by alkali, and than neutralized by acid. The extract were passed through the column of DEAE cellulose for more purification. The neutral fraction was concentrated and precipitated with 95% ethanol. The precipitate was lyophilized and PSG was obtained. The immunomodulating effects of PSG on macrophage were performed by using murine macrophage cell line ATCC TIB 71 cells with PSG 0.5mg. PSG alone could not induce the production of nitrite, but it had a significant potential effect on nitrite secretion when the cells were primed and triggered with BCG and Interferon(IFN)-${\gamma}$. Also it was prominent by using calcium channel blocker(verapamil) and adenylate cyclase activator(forskolin).

• 대한치주과학회:학술대회논문집
• /
• 2001.12a
• /
• pp.63-63
• /
• 2001

• The Korean Journal of Physiology and Pharmacology
• /
• v.2 no.1
• /
• pp.55-62
• /
• 1998

${\alpha},\;{\beta}-Adrenergics$, and calcium channels were known to be related to inducing cardiac hypertrophy. Recently, it was reported that the cardiac renin-angiotensin system (RAS) was an important factor in ventricular hypertrophy. The present study was aimed to investigate the effects of ${\alpha},\;{\beta}-adrenergic$, and calcium channel blockers that might be involved in the regulation of cardiac RAS. The reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of renin gene in the perfused rat heart. Changes in angiotensin converting enzyme (ACE) activity and cyclic AMP (cAMP) content which were thought to play a role in inducing cardiac hypertrophy were measured in the perfused rat heart. The expression of renin gene was not only increased by isoproterenol with metoprolol-pretreatment but also increased by vasopressin treatment in the presence of calcium channel blocker, nifedipine or verapamil. Either prazosin alone or norepinephrine with prazosin-pretreatment significantly increased the ACE activity. However, isoproterenol with metoprolol-pretreatment significantly decreased the ACE activity. On the other hand, the ACE activity was not changed by vasopressin, nifedipine, or verapamil treatments. The content of cAMP was significantly increased by either isoproterenol or vasopressin treatment. According to these results, renin gene expression was associated with ${\beta}2$ - adrenoceptor and calcium channel. ACE activity was associated with ${\alpha}-\;and{\beta}2$ - adrenoceptor. In conclusion, ${\beta}2$ - adrenoceptor was important in cardiac renin gene expression and ACE activity and ${\alpha},\;{\beta}$ -adrenergic, and calcium channel blockers might be involved in the regulation of cardiac RAS in a complicated way.

• Korean Journal of Clinical Pharmacy
• /
• v.30 no.4
• /
• pp.259-263
• /
• 2020

Background: Dual-type calcium channel blockers (CCBs), such as efonidipine and cilnidipine, are renoprotective drugs that reportedly reduce proteinuria by dilating afferent and efferent arterioles of the glomerulus. However, studies comparing the effect of dual-type CCB on proteinuria have not been conducted. Therefore, we aimed to compare the effect of dual-type CCB (efonidipine and cilnidipine) usage patterns in hypertensive patients with chronic kidney disease (CKD). Methods: This single-center, retrospective study included 53 patients with CKD who 1) initiated efonidipine or cilnidipine treatment while on a renin-angiotensin system inhibitor and 2) had received efonidipine or cilnidipine for at least one year. We compared usage patterns between the efonidipine and cilnidipine groups during the one-year period and analyzed the following outcomes: urinary protein-to-creatinine ratio, blood pressure, and serum creatinine. Results: The study included 25 patients in the efonidipine group and 28 patients in the cilnidipine group. In both groups, blood pressure and urinary protein-to-creatinine ratios tended to decrease; however, the change during each interval was not significant. Conclusions: In patients with CKD who were on renin-angiotensin system inhibitor therapy, the addition of a dual-type CCB (i.e., efonidipine or cilnidipine) tended to reduce proteinuria; however, the change during each interval was not significant.

• Journal of Yeungnam Medical Science
• /
• v.32 no.1
• /
• pp.17-21
• /
• 2015

Amlodipine, a calcium channel blocker of the dihydropyridine group, is commonly used in management of hypertension, angina, and myocardial infarction. Amlodipine overdose, characterized by severe hypotension, arrythmias, and pulmonary edema, has seldom been reported in Korean literature. We report on a fatal case of amlodipine intoxication with complications including rhabdomyolysis and oliguric acute kidney injury. A 70-year-old woman with a medical history of hypertension was presented at the author's hospital 6 hours after ingestion of 50 amlodipine (norvasc) tablets (total dosage 250 mg) in an attempted suicide. Her laboratory tests showed a serum creatinine level of 2.5 mg/dL, with elevated serum creatine phosphokinase and myoglobin. The patient was initially treated with fluids, alkali, calcium gluconate, glucagon, and vasopressors without a hemodynamic effect. High-dose insulin therapy was also started with a bolus injection of regular insulin (RI), followed by continuous infusion of RI and 50% dextrose with water. Despite intensive treatment including insulin therapy, inotropics, mechanical ventilation, and continuous venovenous hemodiafiltration, the patient died of refractory shock and cardiac arrest with no signs of renal recovery 116 hours after her hospital admission.

• Journal of Plant Biology
• /
• v.34 no.3
• /
• pp.239-244
• /
• 1991

Ca2+ is implicated as a second messenger in coupling various stimuli such as hormone, gravity and light. The determine whether or not plant hormones mobilize calcium with different action, we investigated the cytosolic Ca2+ changes by IAA and zeatin in the protoplasts isolated from elongating mesocotyl of maize. IAA increased the influx of Ca2+ due to the calcium channel opening, which was confirmed by using verapamil, calcium channel blocker. On the other hand, zeatin increased the cytosolic Ca2+ by promoting the efflux of Ca2+ derived from cellular organelles. These results suggest that different calcium flux induced by IAA and zeatin plays a role in appropriate response resulting in increase of cell elongation or repression cell elongatoin.

• The Korean Journal of Pharmacology
• /
• v.31 no.2
• /
• pp.195-206
• /
• 1995

The study was undertaken to examine the possibility of the involvement of $K^+$ channels in the mechanism of relaxant-action of imipramine on the isolated canine detrusor muscle strips. Canine urinary bladder were isolated, and smooth muscle strips of 15 mm long and 2 mm wide from the mid-portion of anterior wall were made in the Tyrode solution of $0{\sim}4^{\circ}C$. The strips were prepared for isometric myography in Biancani's isolated muscle chamber containing 1 ml of Tyrode solution, which was maintained with pH 7.4 by aeration with $95%\;O_2/5%CO_2\;at\;37^{\circ}C$. RP 52891, a non-specific $K^+$ channel opener, concentration-dependently suppressed the spontaneous phasic contractions of the detrusor strips. Imipramine, a tricyclic antidepressant, also reduced the spontaneous contractions in a concentration-dependent manner. RP 52891 was more potent than imipramine(p<0.05), and Imipramine was more efficient than RP 52891(p<0.05).Procaine, a voltage-dependent $K^+$ channel blocker, glibenclamide, an ATP-dependent $K^+$ channel blocker, and apamin, a calcium-dependent $K^+$ channel blocker antagonized the relaxant effect of RP 52891, but not of imipramine. Imipramine reduced the electric field stimulation (EFS) -induced contractions concentration-dependently. None of the $K^+$ channel blockers employed for this study, procaine, glibenclamide or apamin antagonized the inhibitory action of imipramine on the EFS-induced contraction. These results suggest that in canine detrusor, the $K^+$ channels of the characteristics of voltage-dependent, ATP-dependent and/or calcium-dependent are exist, and the inhibitory action of imipramine on the contractility of the detrusor is independent from the $K^+$ channels.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.16 no.2
• /
• pp.389-396
• /
• 2002

In the present work, we examined the mechanism of vasorelaxant effect of scopoletin, an active constituent of Artemisia capillaris on rat thoracic descending aortic rings. Scopoletin induced a concentration-dependent relaxation in rat thoracic descending aortic rings pre-contracted with phenylephrine (EC/sub 50/ = 238.94±37.4 μM), while it was less effective in rat thoracic descending aortic rings precontracted with high potassium solution (KCI 30 mM). Vasorelaxation by scopoletin was significantly inhibited after endothelial removal, but recovered at high concentration. Pretreatment of rat thoracic descending aortic rings with N/sup G/-nitro-L-arginine (100 μM), a nitric oxide synthase inhibitor, and atropine (1 μM), a muscarinic receptor antagonist, significantly inhibited scopoletin-induced relaxation of rat thoracic descending aortic rings. Neither indomethacin (3 μM), an inhibitor of cydooxygenase, nor propranolol (1 μM), a β -adrenoceptor antagonist, modified the effect of scopoletin. The combination of N/sup G/ -nitro-L-arginine (100 μ M) and miconazole (10 μ M), an inhibitor of cytochrome P 450, did not modify the effect of scopoletin, when compared with pretreatment with N/sup G/-nitro-L-arginine(100 μM) alone. Vasorelaxant effect of scopoletin was inverted by pretreatment with diltiazem (10 μM), a Ca/sup 2+/-channel blocker, at low concentration, while restored at high concentration. Apamin (K/sub ca/-channel blocker, 1 μM), 4-aminopyridine (4-AP, K/sub v/-channel blocker, 1 mM), and tetrodotoxin (TTX, Na/sup +/-channel blocker 1 μM) potentiated the vasorelaxant effect of scopoledn, but glibendamide (K/sub ATP/-channel blocker, 10 μM), tetraetylammonium(TEA, non-selective K-channel blocker, 10 mM) did not affect the relaxation of scopoletin. Free radical scavengers (TEMPO, catalase, mannitol) did not modify vascular tone. These results suggest that nitric oxide, Ca/sup 2+/ -channels play a role in endothelium-dependent relaxations to scopoletin in rat aortas, that apamin, 4-AP, TTX but not glibenclamide, TEA potentiated relaxation to scopoletin mediated by these channels, and that free radicals do not concern to the vasorelaxant effect of scopoletin.