No abstract available.
Amiloride* ; Colon* ; Colonic Neoplasms* ; Humans*

In an attempt to obtain evidence in the mechanism of stone formation, the effectiveness of Amiloride. a K-sparing diuretic known to act on the distal nephron. on the kidney with oxamide-induced urolithiasis was investigated. Futhermore. the influence of stone formation on the distribution of intrarenal blood flow and the effect of Amiloride on them were also studied. Most prominent derangements of renal function observed during stone formation were decreases of both C(PAH) and C(cr) indicating the curtailment in renal hemodynamics. The oxamide-treated kidney also responded to Amiloride with typical natriuresis and antikaluresis. in the same fashion with normal kidneys. The experiments in which the intrarenal blood flow distribution was measured by PAH-extraction technique raveled that mainly the cortical blood flow was curtailed, whereas non-cortical blood flow (medullary flow) did not change during oxamide-stone formation. Amiloride did not influence the intrarenal b100d flow distribution both in normal and oxamide kidneys. These observations suggest that oxamide-stone formation was initiated not by tubular necrosis produced by the toxic action of oxalate on the tubules, but rather by mechanical obstruction of the tubules.
Amiloride* ; Hemodynamics ; Kidney* ; Natriuresis ; Necrosis ; Nephrons ; Renal Circulation ; Urolithiasis

In order to investigate electrolyte changes in serum and urine diuretic therapy, we studied 98 patients with hypertension not optimally controlled by previous treatment. After we divied the patients into three gorups in randomized trial, group A were given Amiloride 10mg/day, group B were given Dihydrochlorothiazide 50mg/day, group C were given Amiloride 5mg/day combined with Dihydrochlorothiazide 25mg/day for 7 days. Blood pressure and electrolyte changes in serum and urine after diuretic theraphy for 7 days were as follows. 1) Serum sodium concentrations were not significantly changed in all three groups(P>0.05). 2) Serum potassium concentrations were increased in group A and C (P<0.05), but there were no significant changes in group B(P<0.05). 3) Urinary sodium exceretions were increased in all three groups(P<0.05). 4) Urinary potassium excretion were decreased in group A and C (P<0.05), but there were increased in group B (P<0.05). 5) Blood pressure were decreased in all three groups(P<0.05).
Amiloride ; Blood Pressure ; Diuretics* ; Electrolytes* ; Humans ; Hydrochlorothiazide ; Hypertension* ; Potassium ; Sodium

PURPOSE: In the present study the effects of amiloride on the growth of human gastric adenocarcinoma cell line, AGS cells were examined with or without the addition of 5-fluorouracil (5-FU) in vitro. MATERIALS AND METHODS: The growth of AGS cells was examined by counting number of cells on two and four days post-treatment with 50 micrometer, 100 micrometer, 200 micrometer, 400 micrometer, 800 micrometer, amiloride, and 0.1 microgram/ml, 0.3 microgram/ml 5-FU, after plating AGS cells into 6 well plates at a density of 10 x 10(4) cells/well. The reversibility of the effects of amiloride was examined on two to eight days post-treatment with 400 micrometer amiloride after seeding 2 x 10(4) cells/dish. Cell cycle analysis was performed after four day-treatment with 400 micrometer amiloride. RESULTS: Amiloride (50~800 micrometer) significantly inhibited the growth of AGS in a dose-dependent fashion (p<0.05). The inhibitory effect of amiloride on growth of AGS was reversible since removal of amiloride after 24 hours treatment led to resumption of rapid growth up to control levels. Amiloride combined with 5-FU markedly inhibited the growth of AGS in a dose-dependent fashion compared to that of amiloride or 5-FU alone (p<0.05). The fraction of S phase, G0-G1 phase and G2-M phase was 19.3%, 55.7%, 18.8%, in the amioride group (400 micrometer) and 43.9%, 37.4%, 25.1% in the control group, respectively, showing significantly higher G1 fraction in amiloride group compared to control. CONCLUSION: This is the first paper which reported that amiloride inhibited in vitro growth of human gastric adenocarcinoma cells and that its effect of growth inhibition may be synergistic with 5-FU. Amiloride given with or without 5-FU may be useful agent in the treatment of gastric carcinomas. The inhibitory effects of amiloride on the growth of AGS may be mediated in part by blocking G1-S transition of cell cycle.
Adenocarcinoma ; Amiloride* ; Cell Cycle ; Cell Line ; Fluorouracil ; Humans* ; S Phase

BACKGROUND AND OBJECTIVES: Rhinovirus infection on the airway epithelial cells results in derangement in mucociliary clearance. However, the contribution of altered ion transport across the epithelial cells in rhinovirus-induced alteration in mucociliary clearance has not been studied yet. Thus, we aimed to investigate the effect of rhinovirus infection on the electrical property of airway epithelial cells. MATERIALS AND METHODS: Tracheal mucosae were harvested and digested with protease. The epithelial cells thus obtained were cultured in air-liquid interface method. Rhinvovirus-16s were infected for 1 hour on the epithelial cells and cultured for 48 hours thereafter. Transepithelial resistance was measured by a chopstick voltmeter and short circuit current was measured by Ussing chamber technique. The electrical properties of control and infection groups were compared. RESULTS: The change in the transepithelial resistance in the control group was 240 ohm.cm2, while it was 263 ohm.cm2 in the RV infected epithelium. The baseline short circuit current was 6.3 microEq.cm-2.h-1 in the control group and 7.2 microEq.cm-2.h-1 in the RV infected group. The difference was not significant. Change in short circuit current induced by mucosally applied amiloride and foskolin were not different significantly in both groups. CONCLUSION: The results of this study indicated that rhinovirus infection in the airway epithelial cells does not affect the electrical property, which reflects the function of ion channels in the epithelial cells.
Amiloride ; Epithelial Cells* ; Epithelium ; Ion Channels ; Ion Transport ; Mucociliary Clearance ; Mucous Membrane ; Rhinovirus

Severe hyperkalemia can induce life threatening cardiac rhythm disturbances, and usually produce classic electrocardiographic (EKG) manifestations. We report a case of severe hyperkalemia in which the EKG did not reveal the expected alterations. The patient was a 57-year-old man with adenocarcinoma of stomach. There were no significant abnormal findings in laboratory analysis, chest X-ray and EKG. His preoperative medications for hypertension consisted of furosemide, amiloride and enalapril. The tests for serum potassium concentration ([K ]) were performed on 20 and 7 days before the operation and the results were 4.5 and 4.9 mEq/l, respectively. Just after induction of anesthesia, we tried the blood gas and electrolyte analysis and the result revealed high [K ] of 8.5 mEq/l, but EKG did not show typical phenotype of hyperkalemia at that time. His intraoperative and postoperative courses were not eventful.
Adenocarcinoma ; Amiloride ; Anesthesia ; Electrocardiography* ; Enalapril ; Furosemide ; Humans ; Hyperkalemia* ; Hypertension ; Ions ; Middle Aged ; Phenotype ; Potassium ; Stomach ; Thorax

The rabbit cornea was studied in vitro in modified Ussing chambers to determine the effects of ion transport inhibitors and hydrogen peroxide(H2O2) on ion transport through the cornea by measuring the bioelectric properties. Apical(tear side, T side) addition of furosemide, bumetanide and SITS were ineffective on resting Isc(short circuit current). Apical addition of 1.0mM amiloride(Na+/H+ antiport inhibitor) and NPAA(Cl- channel blocker) markedly reduced the resting Isc, but basolateral(stromal side, S side) addition of amiloride was ineffective. The site of action of these agents was the apical membrane. H2O2, an oxygen free radical, markedly increased the lsc when was added to the T side, but S side addition of the H2O2 was ineffective. To determine the degree of cellular catalase participation in protection against H2O2 induced injury the cornea was pretreated with ATAZ for 30 min prior to H2O2 action. The increase of lsc by H2O2 was markedly potentiated after pretreatment with ATAZ on T side compared to that of S side addition. This result indicates that the corneal endothelial H2O2 may be largely degraded by catalase. When H2O2 was added to the T side, Isc was raised by increased ion transport. All ion transport inhibitors that were used inhibited the H2O2 effect on Isc. Moreover, amiloride and NPAA markedly inhibited induced lsc by H2O2. These results suggest that H2O2 stimulates the corneal epithelial ion transport and that its site of action is apical membrane Na+/H+ antiport system and CI- channel system.
4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid ; Amiloride ; Bumetanide ; Catalase ; Cornea ; Furosemide ; Hydrogen Peroxide* ; Hydrogen* ; Ion Transport ; Membranes ; Oxygen

Liddle's syndrome is a rare inherited disease with characteristic clinical manifestations of hypertension and hypokalemic metabolic alkalosis. Markedly suppressed serum aldosterone and renin levels are important laboratory findings to differentiate this disorder from primary hyperaldosteronism. When Liddle et al. reported the disorder in 1963, they proposed aggressive Na+ absorption and increased excretion of K+ as the pathogenesis of the syndrome. Since then, specific mutation in the epithelial Na+ channel located in the collecting duct of the kidney has been elucidated as a disease mechanism. Liddle's syndrome is inherited by an autosomal dominant trait and generally the onset of the syndrome is before the age of 20 with increased risk of premature death due to stroke or heart failure. Recently, however, a few cases of late onset and genetically proven nonfamilial cases with de novo mutation of beta or gamma Na+ channel have been reported. We report a case of seventy-one year old woman who had hypertension with hypokalemic metabolic alkalosis and was diagnosed as Liddle's syndrome. Further evaluation revealed low serum renin and aldosterone levels. Primary aldosteronism, Cushing's syndrome, glucocorticoid remediable aldosteronism and deficiency of 11beta-OHase and 17alpha-OHase were ruled out based on her laboratory data and history. Her hypertension and hypokalemia responded to amiloride treatment but not to spironolactone.
Absorption ; Aldosterone ; Alkalosis ; Amiloride ; Cushing Syndrome ; Female ; Heart Failure ; Humans ; Hyperaldosteronism ; Hypertension ; Hypokalemia ; Kidney ; Mortality, Premature ; Renin ; Spironolactone ; Stroke

Gap junction protein, connexin, is expressed in endothelial cells of vessels, glomerulus, and renin secreting cells of the kidney. The purpose of this study was to investigate the role of gap junction in renin secretion and its underlying mechanisms using As 4.1 cell line, a renin-expressing clonal cell line. Renin release was increased proportionately to incubation time. The specific gap junction inhibitor, 18-beta glycyrrhetinic acid (GA) increased renin release in dose-dependent and time- dependent manners. Heptanol and octanol, gap junction blockers, also increased renin release, which were less potent than GA. GA-stimulated renin release was attenuated by pretreatment of the cells with amiloride, nifedipine, ryanodine, and thapsigargin. GA dose-dependently increased intracellular Ca2+ concentration, which was attenuated by nifedipine, nimodipine, ryanodine, and thapsigargin. However, RP-cAMP, chelerythrine, tyrphostin A23, or phenylarsine oxide did not induced any significant change in GA-stimulated increase of intracellular Ca2+ concentration. These results suggest that gap junction plays an important role on the regulation of renin release and intracellular Ca2+ concentration in As 4.1 cells.
Amiloride ; Calcium* ; Cell Line* ; Connexins ; Endothelial Cells ; Gap Junctions* ; Glycyrrhetinic Acid ; Heptanol ; Kidney ; Nifedipine ; Nimodipine ; Renin* ; Ryanodine ; Thapsigargin

Cells can resist and even recover from stress induced by acute hypoxia, whereas chronic hypoxia often leads to irreversible damage and eventually death. Although little is known about the response(s) to acute hypoxia in neuronal cells, alterations in ion channel activity could be preferential. This study aimed to elucidate which channel type is involved in the response to acute hypoxia in rat pheochromocytomal (PC12) cells as a neuronal cell model. Using perfusing solution saturated with 95% N2 and 5% CO2, induction of cell hypoxia was confirmed based on increased intracellular Ca2+ with diminished oxygen content in the perfusate. During acute hypoxia, one channel type with a conductance of about 30 pS (2.5 pA at -80 mV) was activated within the first 2~3 min following onset of hypoxia and was long-lived for more than 300 ms with high open probability (Po, up to 0.8). This channel was permeable to Na+ ions, but not to K+, Ca+, and Cl- ions, and was sensitively blocked by amiloride (200 nM). These characteristics and behaviors were quite similar to those of epithelial sodium channel (ENaC). RT-PCR and Western blot analyses confirmed that ENaC channel was endogenously expressed in PC12 cells. Taken together, a 30-pS ENaC-like channel was activated in response to acute hypoxia in PC12 cells. This is the first evidence of an acute hypoxia-activated Na+ channel that can contribute to depolarization of the cell.
Amiloride ; Animals ; Anoxia ; Blotting, Western ; Cell Hypoxia ; Epithelial Sodium Channels ; Ion Channels ; Ions ; Neurons ; Oxygen ; PC12 Cells ; Pheochromocytoma ; Rats