• 약학회지
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• 제36권1호
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• pp.46-55
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• 1992

Methoxyverapamil, $Ca^{2+}$ channel blocker, when given intravenously by means of bolus, produced the transient increase of urine flow, and then methoxyverapamil was infused in this experiments. Methoxyverapamil, when infused into vein, elicited the increase of urine flow ancampanied with the increased glomeralar filtration rate(GFR), renal plasma flow(RPF), excretion amounts of sodium and potassium in urine($E_{Na},\;E_k$) and osmolar clearance(Cosm), wherease produced the no change of free water clearance($C_{H2O}$) and the reduction of reabsorption rates of sodium and potassium in reral tubules($R_{Na},\;R_k$). Methoxyverapamil, when infused into a renal artery, exhibited the diuretic action in only infused Kidney, at this time changes of renal function were the same aspect to that of intravenously infused methoxyverapamil. Methoxyverapamil, when infused into a carotid artery, exhibited the decreased urine flow along with the reduction of Cosm, $C_{H2O}\;and\;E_{Na}$. Above results suggest that methoxyverapamil possess both the diuretic action by direct action in kidney and antidiuretic action through the central function.

• Bulletin of the Korean Chemical Society
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• 제32권7호
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• pp.2274-2278
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• 2011

Verapamil is a calcium channel blocker and is classified as a class IV anti-arrhythmic agent. It is used in the control of supra ventricular tachyarrhythmias, and in the management of classical and variant angina pectoris. It is also used in the treatment of hypertension and used as an important therapeutic agent for angina pectoris, ischemic heart disease, hypertension and hypertrophic cardiomyopathy. Verapamil commonly co-administered with NSAIDs (non-steroidal anti-inflammatory drugs) i.e. diclofenac sodium, flurbiprofen, Ibuprofen, mefanamic acid and meloxicam. A simple and rapid RP-HPLC method for simultaneous determination and quantification of verapamil and NSAIDs was developed and validated. The mobile phase constituted of acetonitrile: water (55:45) whose pH was adjusted at 2.7 and pumped at a flow rate of 2.0 mL $min^{-1}$ at 230 nm. The proposed method is simple, precise, accurate, low cost and least time consuming for the simultaneous determination of verapamil and NSAIDs which can be effectively applied for the analysis of human serum.

• 한국수산과학회지
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• 제29권6호
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• pp.856-861
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• 1996

The occurrence of TTX in ciliated protozoa was investigated in order to clarify tetrodotoxin (TTX) accumulation mechanisms in marine organisms. Tissue culture bioassay, HPLC, and GC-MS analyses confirmed the occurrence of TTX in Euplotes mutabilis and also in bacteria isolated from the culture medium. Fluorescently labeled bacteria (FLB) were prepared with those bacteria, and predation by E. mutabilis was observed. The results indicated that TTX in bacteria can be transferred to higher trophic levels through the food chain.

• 환경생물
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• 제18권2호
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• pp.255-262
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• 2000

Synaptosome에 의한 [$^3$H]-serotonin의 일반적인 흡수특성과 이 과정에 납이 미치는 영향을 in vitro와 in vitro에서 관찰하였다. 흰쥐의 대뇌와 뇌간에서 각각 분리한 synaptosome의 흡수친화력은 대뇌가 Km=0.5$\mu$M, 뇌간이 Km=0.1$\mu$M로 모두 고친화성 흡수였고 뇌간에서 더 높았다. 또한 이 흡수과정에 sodium과 potassium이온이 영향을 미치는 것으로 나타났다. Synaptosome이 [$^3$H]-serotonin을 흡수하는 과정은 납에 의해 억제되었고 이러한 납의 독성영향은 in vitro와 in vitro에서 유사한 결과를 보였다.

• The Korean Journal of Physiology
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• 제24권1호
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• pp.115-121
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• 1990

Pentobarbital 마취한 정상혈압 및 신성 고혈압 흰쥐에서 calcium channel 봉쇄 약물 nifedipine과 atrial natriuretic peptide(ANP)의 상호작용을 조사하였다. 정상혈압 흰쥐에서 nifedipine$(1.0\;{\mu}g/kg/min)$ 또는 ANP(60 ng/kg/min)의 주입은 각각 유의하게 혈압을 내렸으며 두 약물의 동시 주입시에 개별적으로 주입하였을 때보다 그 혈압내림의 정도가 더욱 컸다. Nifedipine은 단독 주입하였을 때에 신기능에 유의한 영향을 미치지 않았으나 ANP와 동시에 주입하였을 때에는 ANP의 요량 및 Na 배설 증가 효과를 항진시켰다. 한편 고혈압 흰쥐에서도 ANP의 혈압내림효과와 신장효과는 nifedipine과 함께 주입하였을 때에 더 컸다. 적출 흉부대동맥 표본을 phenylephrine으로 미리 수축시킨 후 ANP를 첨가하면 용량의존 이완반응을 보였고 nifedipine 존재하에서 더 예민하였다. 이상의 실험결과는 calcium channel 봉쇄약물이 ANP의 혈압내림효과를 항진시킴을 보인 것이며 그 기전으로 요중 배설 증가 및 혈관이완효과 증가 등이 관여함을 시사하였다.

• Journal of Chest Surgery
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• 제18권1호
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• pp.1-6
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• 1985

Isolated sinus node cells of the rabbit were used to assess the effects of extracellular Na, K, Ca and Mg concentrations on cardiac pacemaker activity. With intracellular glass micro-electrodes spontaneous action potentials of SA node were recorded and the effects of various ions and their blockers were analyzed in terms of the cycle length, the amplitude and the duration of action potentials, the results obtained were as follows. 1. Sodium reduction [up to 30%] decreased the amplitude of action potential and lengthened the cycle length. TTX, specific blocker of Na channel slightly lengthened the cycle length. 2. Increasing potassium ion concentration, the duration of action potential decreased and the frequency increased in 6mM, however, spontaneous action potential was stopped in 24 mM. Barium ion known to be decreasing K conductance increased the duration of action potential but no significant change in the cycle length was noticed. 3. Calcium ion has shortening effect on the duration and the cycle length of action potential but not with dose-dependent manner. Cadmium ion .[0.02mM] lengthened cycle length and the duration of action potential. 4. Increasing the concentration of magnesium ion the cycle length was lengthened, significantly.

• Asian Pacific Journal of Cancer Prevention
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• 제16권2호
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• pp.831-836
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• 2015

Tumor fluid accumulation occurs in both human cancer and experimental tumor models. Solid tumors show a tendency to tumor fluid accumulation because of their anatomical and physiological features and this may be influenced by molecular factors. Fluid accumulation in the peri-tumor area also occurs in the Dunning model of rat prostate cancer as the tumor grows. In this study, the effects of tumor fluids that were obtained from Dunning prostate tumor-bearing Copenhagen rats on the strongly metastatic MAT-LyLu cell line were investigatedby examining the cell's migration and tumor fluid's toxicity and the kinetic parameters such as cell proliferation, mitotic index, and labelling index. In this research, tumor fluids were obtained from rats injected with $2{\times}10^5$ MAT-LyLu cells and treated with saline solution, and 200 nM tetrodotoxin (TTX), highly specific sodium channel blocker was used. Sterilized tumor fluids were added to medium of MAT-LyLu cells with the proportion of 20% in vitro. Consequently, it was demonstrated that Dunning rat prostate tumor fluid significantly inhibited proliferation (up to 50%), mitotic index, and labeling index of MAT-LyLu cells (up to 75%) (p<0.05) but stimulated the motility of the cells in vitro.

• Journal of Plant Biotechnology
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• 제34권3호
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• pp.213-221
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• 2007

분리된 무 자엽 조직에 산화질소 (nitric oxide: NO) 공여체인 sodium nitroprusside (SNP) 처리 시 농도 의존방식으로 부정근의 발달을 증진시켰다. 그러나 이러한 NO 증진 효과는 세포외 칼슘 chelator인 0.5 mM EGTA 또는 세포막 칼슘채널 차단제인 0.1 mM $LaCl_3$를 각각 $50\;{\mu}M$ SNP와 함께 혼합처리 시 반전되었다. 또한, 뿌리 발생에서 중심적 역할을 수행하는 것으로 알려진 guaiacol peroxidase (GPX)와 syringaldazine peroxidase (SPX)의 활성도가 SNP 단독 처리된 자엽에서 부정근이 형성되는 동안 현저히 증가하였다. 그러나, SNP와 $LaCl_3$ 혼합처리 시 SNP에 의해 유도된 GPX와 SPX 활성도 증가가 거의 증류수 대조구 수준으로 억제되었다. calmodulin의 anatagonist인 trifuoperazine 역시 SNP로 처리된 자엽에서 부정근 형성을 억제하여 발생된 뿌리의 개수와 길이를 감소시켰으며 동시에 GPX와 SPX를 불활성화 하였다. 결론적으로, 이들 결과는 칼슘이 GPX와 SPX 활성도 조절을 통해 부정근 유도를 이끄는 NO 반응에 포함되어 있음을 나타내는 것이다.

• Biomolecules & Therapeutics
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• 제8권1호
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• pp.13-21
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• 2000

The present study was designed to investigate the effect f quinidine on catecholamine (CA) secretion evoked by ACh, high $K^{+}$, DMPP, McN-A343, cyclopiazonic acid and Bay-K-8644 from the isolated perfused rat adrenal gland and to establish the mechanism of its action. The perfusion of quinidine (15-150 $\mu$M) into an adrenal vein for 60 min produced relatively dose- and time-dependent inhibition in CA secretion evoked by ACh (5.32$\times$10$^{-3}$ M), high $K^{+}$ (5.6$\times$10$^{-2}$ M), 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). Furthermore, in adrenal glands pre-loaded with quinine (5$\times$10$^{-5}$ M), CA secretory responses evoked by veratridine (10$^{-4}$ M) was time-dependently inhibited. Also, in the presence of lidocaine (10$^{-4}$ M), which is also known to be a sodium channel blocker, CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclo-piazonic acid were also greatly reduced in similar fashion to that of quinidine-treatment. Taken together, these results suggest that quinidine causes greatly the inhibition of CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization, indicating strongly that this effect may be mediated by inhibiting influx of extracellular calcium and release in intracellular calcium in the rat adrenomedullary chromaffin cells. Furthermore, these findings indicate strongly that this inhibitory action of quinidine appears to be associated to the blocking action of sodium channels at least in CA secretion from the rat adrenal gland.and.

• Archives of Pharmacal Research
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• 제14권3호
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• pp.242-248
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• 1991

Antihypertensive effect of YH 334 was examined in various experimental hypertension rat models and the systemic and regional hymohynamic profiles of the compound were investigated in conscious spontaneously hypertensive rats (SHR). The antiypertensive potensive potency of YH 334 is found to be more than 10 times stronger than that of nitrendipine in the all hypertensive models. The effective doses to lower the initial blood pressure by 20% $(ED_{20})$ of YH334 were 1.4 mg/kg in normotensive rats (NR), 0.7 mglkg in SHR. 0.1 mg/kg in DOCA salt hypertensive rats (DHR) and 0.4 mg/kg in renal hypertensive rats (RHR), and the $ED_{20}$ values of nitrendipine were 15.8 mg/kg in NR, 7.1 mg/kg in SHR, 1.7 mg/kg in DHR and 4.8 mg/kg in RHR. The primary hemodynamic effect hemodynamic profile is similar to that of nitrendipine. Both compounds seem to produce potent antihypertensive effects by lowering peripheral resistance in the skeletal muscles. In the organ bath study using isolated rabbit aorta, YH 334 was found to be a potent voltage dependent calcium channel blocker without significant inhibitory effect on the receptor operated calcium channels like the most of other dihydropyridine type calcium antagonists. Furthermore, YH334 showed acute diuretic and natriuretic effects in conscious SHR, which may render the unnecessary restriction of sodium in the diet of those patients on long term hypertension therapy. This effect would provide an additional benefit to its potent antihypertensive activity.