Benzolamide: Selective renal carbonic anhydrase inhibitor. It may also be of use in certain cases of respiratory failure.Carbonic Anhydrase Inhibitors: A class of compounds that reduces the secretion of H+ ions by the proximal kidney tubule through inhibition of CARBONIC ANHYDRASES.Ethoxzolamide: A carbonic anhydrase inhibitor used as diuretic and in glaucoma. It may cause hypokalemia.Carbonic Anhydrases: A family of zinc-containing enzymes that catalyze the reversible hydration of carbon dioxide. They play an important role in the transport of CARBON DIOXIDE from the tissues to the LUNG. EC 4.2.1.1.Carbonic Anhydrase IV: A membrane-bound carbonic anhydrase found in lung capillaries and kidney.Methazolamide: A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma.Bicarbonates: Inorganic salts that contain the -HCO3 radical. They are an important factor in determining the pH of the blood and the concentration of bicarbonate ions is regulated by the kidney. Levels in the blood are an index of the alkali reserve or buffering capacity.Acetazolamide: One of the CARBONIC ANHYDRASE INHIBITORS that is sometimes effective against absence seizures. It is sometimes useful also as an adjunct in the treatment of tonic-clonic, myoclonic, and atonic seizures, particularly in women whose seizures occur or are exacerbated at specific times in the menstrual cycle. However, its usefulness is transient often because of rapid development of tolerance. Its antiepileptic effect may be due to its inhibitory effect on brain carbonic anhydrase, which leads to an increased transneuronal chloride gradient, increased chloride current, and increased inhibition. (From Smith and Reynard, Textbook of Pharmacology, 1991, p337)Kidney Tubules: Long convoluted tubules in the nephrons. They collect filtrate from blood passing through the KIDNEY GLOMERULUS and process this filtrate into URINE. Each renal tubule consists of a BOWMAN CAPSULE; PROXIMAL KIDNEY TUBULE; LOOP OF HENLE; DISTAL KIDNEY TUBULE; and KIDNEY COLLECTING DUCT leading to the central cavity of the kidney (KIDNEY PELVIS) that connects to the URETER.Altitude Sickness: Multiple symptoms associated with reduced oxygen at high ALTITUDE.Mountaineering: A sport involving mountain climbing techniques.Altitude: A vertical distance measured from a known level on the surface of a planet or other celestial body.Expeditions: Usually refers to planned scientific data-gathering excursions.Atmosphere Exposure Chambers: Experimental devices used in inhalation studies in which a person or animal is either partially or completely immersed in a chemically controlled atmosphere.Cardiology: The study of the heart, its physiology, and its functions.Sleep Medicine Specialty: A medical specialty concerned with the diagnosis and treatment of SLEEP WAKE DISORDERS and their causes.Emergency Medicine: The branch of medicine concerned with the evaluation and initial treatment of urgent and emergent medical problems, such as those caused by accidents, trauma, sudden illness, poisoning, or disasters. Emergency medical care can be provided at the hospital or at sites outside the medical facility.Gastroenterology: A subspecialty of internal medicine concerned with the study of the physiology and diseases of the digestive system and related structures (esophagus, liver, gallbladder, and pancreas).Endocrinology: A subspecialty of internal medicine concerned with the metabolism, physiology, and disorders of the ENDOCRINE SYSTEM.Nephrology: A subspecialty of internal medicine concerned with the anatomy, physiology, and pathology of the kidney.Neurology: A medical specialty concerned with the study of the structures, functions, and diseases of the nervous system.HEPES: A dipolar ionic buffer.Membrane Potentials: The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).Patch-Clamp Techniques: An electrophysiologic technique for studying cells, cell membranes, and occasionally isolated organelles. All patch-clamp methods rely on a very high-resistance seal between a micropipette and a membrane; the seal is usually attained by gentle suction. The four most common variants include on-cell patch, inside-out patch, outside-out patch, and whole-cell clamp. Patch-clamp methods are commonly used to voltage clamp, that is control the voltage across the membrane and measure current flow, but current-clamp methods, in which the current is controlled and the voltage is measured, are also used.Electric Impedance: The resistance to the flow of either alternating or direct electrical current.Microelectrodes: Electrodes with an extremely small tip, used in a voltage clamp or other apparatus to stimulate or record bioelectric potentials of single cells intracellularly or extracellularly. (Dorland, 28th ed)Amplifiers, Electronic: Electronic devices that increase the magnitude of a signal's power level or current.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.Pyramidal Cells: Projection neurons in the CEREBRAL CORTEX and the HIPPOCAMPUS. Pyramidal cells have a pyramid-shaped soma with the apex and an apical dendrite pointed toward the pial surface and other dendrites and an axon emerging from the base. The axons may have local collaterals but also project outside their cortical region.Hippocampus: A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.Electric Stimulation: Use of electric potential or currents to elicit biological responses.IndianaPeriodicals as Topic: A publication issued at stated, more or less regular, intervals.Encephalitis Virus, Murray Valley: A species of FLAVIVIRUS, one of the Japanese encephalitis virus group (ENCEPHALITIS VIRUSES, JAPANESE), found in Australia and New Guinea. It causes a fulminating viremia resembling Japanese encephalitis (ENCEPHALITIS, JAPANESE).Bibliometrics: The use of statistical methods in the analysis of a body of literature to reveal the historical development of subject fields and patterns of authorship, publication, and use. Formerly called statistical bibliography. (from The ALA Glossary of Library and Information Science, 1983)Publications: Copies of a work or document distributed to the public by sale, rental, lease, or lending. (From ALA Glossary of Library and Information Science, 1983, p181)Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.Carbonic Anhydrase II: A cytosolic carbonic anhydrase isoenzyme found widely distributed in cells of almost all tissues. Deficiencies of carbonic anhydrase II produce a syndrome characterized by OSTEOPETROSIS, renal tubular acidosis (ACIDOSIS, RENAL TUBULAR) and cerebral calcification. EC 4.2.1.-Crystallography, X-Ray: The study of crystal structure using X-RAY DIFFRACTION techniques. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Isoenzymes: Structurally related forms of an enzyme. Each isoenzyme has the same mechanism and classification, but differs in its chemical, physical, or immunological characteristics.Factor IX: Storage-stable blood coagulation factor acting in the intrinsic pathway. Its activated form, IXa, forms a complex with factor VIII and calcium on platelet factor 3 to activate factor X to Xa. Deficiency of factor IX results in HEMOPHILIA B (Christmas Disease).Intraocular Pressure: The pressure of the fluids in the eye.Blood-Aqueous Barrier: The selectively permeable barrier, in the EYE, formed by the nonpigmented layer of the EPITHELIUM of the CILIARY BODY, and the ENDOTHELIUM of the BLOOD VESSELS of the IRIS. TIGHT JUNCTIONS joining adjacent cells keep the barrier between cells continuous.Dichlorphenamide: A carbonic anhydrase inhibitor that is used in the treatment of glaucoma.Pregnancy Complications: Conditions or pathological processes associated with pregnancy. They can occur during or after pregnancy, and range from minor discomforts to serious diseases that require medical interventions. They include diseases in pregnant females, and pregnancies in females with diseases.Maternal Mortality: Maternal deaths resulting from complications of pregnancy and childbirth in a given population.Pregnancy: The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.Diagnostic Errors: Incorrect diagnoses after clinical examination or technical diagnostic procedures.Pregnancy Complications, Cardiovascular: The co-occurrence of pregnancy and a cardiovascular disease. The disease may precede or follow FERTILIZATION and it may or may not have a deleterious effect on the pregnant woman or FETUS.Pelvic Girdle Pain: Discomfort associated with the bones that make up the pelvic girdle. It occurs frequently during pregnancy.Puerperal Disorders: Disorders or diseases associated with PUERPERIUM, the six-to-eight-week period immediately after PARTURITION in humans.

Does gill boundary layer carbonic anhydrase contribute to carbon dioxide excretion: a comparison between dogfish (Squalus acanthias) and rainbow trout (Oncorhynchus mykiss). (1/30)

In vivo experiments were conducted on spiny dogfish (Squalus acanthias) and rainbow trout (Oncorhynchus mykiss) in sea water to determine the potential role of externally oriented or gill boundary layer carbonic anhydrase in carbon dioxide excretion. This was accomplished by assessing pH changes in expired water using a stopped-flow apparatus. In dogfish, expired water was in acid-base disequilibrium as indicated by a pronounced acidification (delta pH=-0.11+/-0.01; N=22; mean +/- s.e.m.) during the period of stopped flow; inspired water, however, was in acid-base equilibrium (delta pH=-0.002+/-0.01; N=22). The acid-base disequilibrium in expired water was abolished (delta pH=-0.005+/-0.01; N=6) by the addition of bovine carbonic anhydrase (5 mg l-1) to the external medium. Addition of the carbonic anhydrase inhibitor acetazolamide (1 mmol l-1) to the water significantly reduced the magnitude of the pH disequilibrium (from -0.133+/-0.03 to -0.063+/-0.02; N=4). However, after correcting for the increased buffering capacity of the water caused by acetazolamide, the acid-base disequilibrium during stopped flow was unaffected by this treatment (control delta [H+]=99.8+/-22.8 micromol l-1; acetazolamide delta [H+]=81.3+/-21.5 micromol l-1). In rainbow trout, expired water displayed an acid-base disequilibrium (delta pH=0.09+/-0.01; N=6) that also was abolished by the application of external carbonic anhydrase (delta pH=0.02+/-0.01). The origin of the expired water acid-base disequilibrium was investigated further in dogfish. Intravascular injection of acetazolamide (40 mg kg-1) to inhibit internal carbonic anhydrase activity non-specifically and thus CO2 excretion significantly diminished the extent of the expired water disequilibrium pH after 30 min (from -0.123+/-0.01 to -0.065+/-0.01; N=6). Selective inhibition of extracellular carbonic anhydrase activity using a low intravascular dose (1.3 mg kg-1) of the inhibitor benzolamide caused a significant reduction in the acid-base disequilibrium after 5 min (from -0.11+/-0.01 to -0.07+/-0. 01; N=14). These results demonstrate that the expired water acid-base disequilibrium originates, at least in part, from excretory CO2 and that extracellular carbonic anhydrase in dogfish may have a significant role in carbon dioxide excretion. However, externally oriented carbonic anhydrase (if present in dogfish) plays no role in catalysing the hydration of the excretory CO2 in water flowing over the gills and thus is unlikely to facilitate CO2 excretion.  (+info)

Endogenous pH shifts facilitate spreading depression by effect on NMDA receptors. (2/30)

Rapid extracellular alkalinizations accompany normal neuronal activity and have been implicated in the modulation of N-methyl-D-aspartate (NMDA) receptors. Particularly large alkaline transients also occur at the onset of spreading depression (SD). To test whether these endogenous pH shifts can modulate SD, the alkaline shift was amplified using benzolamide, a poorly permeant inhibitor of interstitial carbonic anhydrase. SD was evoked by microinjection of 1.2 M KCl into the CA1 stratum radiatum of rat hippocampal slices and recorded by a proximal double-barreled pH microelectrode and a distal potential electrode. In Ringer solution of pH 7.1 containing picrotoxin (but not at a bath pH of 7.4), addition of 10 microM benzolamide increased the SD alkaline shift from 0.20 +/- 0.07 to 0.38 +/- 0.17 unit pH (means +/- SE). This was correlated with a significant shortening of the latency and an increase in the conduction velocity by 26 +/- 16%. In the presence of the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (APV), benzolamide still amplified the alkaline transient, however, its effect on the SD latency and propagation velocity was abolished. The intrinsic modulation of SD by its alkaline transient may play an important role under focal ischemic conditions by removing the proton block of NMDA receptors where interstitial acidosis would otherwise limit NMDA receptor activity.  (+info)

Temporal adjustment of the juxtaglomerular apparatus during sustained inhibition of proximal reabsorption. (3/30)

Tubuloglomerular feedback (TGF) stabilizes nephron function by causing changes in single-nephron GFR (SNGFR) to compensate for changes in late proximal flow (VLP). TGF responds within seconds and reacts over a narrow range of VLP that surrounds normal VLP. To accommodate sustained increases in VLP, TGF must reset around the new flow. We studied TGF resetting by inhibiting proximal reabsorption with benzolamide (BNZ; administered repeatedly over a 24-hour period) in Wistar-Froemter rats. BNZ acutely activates TGF, thereby reducing SNGFR. Micropuncture was performed 6-10 hours after the fourth BNZ dose, when diuresis had subsided. BNZ caused glomerular hyperfiltration, which was prevented with inhibitors of macula densa nitric oxide synthase (NOS). Because of hyperfiltration, BNZ increased VLP and distal flow, but did not affect the basal TGF stimulus (early distal salt concentration). BNZ slightly blunted normalized maximum TGF response and the basal state of TGF activation. BNZ sensitized SNGFR to reduction by S-methyl-thiocitrulline (SMTC) and caused the maximum TGF response to be strengthened by SMTC. Sensitization to type I NOS (NOS-I) blockers correlated with increased macula densa NOS-I immunoreactivity. Tubular transport measurements confirmed that BNZ affected TGF within the juxtaglomerular apparatus. During reduced proximal reabsorption, TGF resets to accommodate increased flow and SNGFR through a mechanism involving macula densa NOS.  (+info)

Acid-base effects on electrolyte transport in CA II-deficient mouse colon. (4/30)

To determine the role of carbonic anhydrase (CA) in colonic electrolyte transport, we studied Car-2(0) mice, mutants deficient in cytosolic CA II. Ion fluxes were measured under short-circuit conditions in an Ussing chamber. CA was analyzed by assay and Western blots. In Car-2(0) mouse colonic mucosa, total CA activity was reduced 80% and cytosolic CA I and membrane-bound CA IV activities were not increased. Western blots confirmed the absence of CA II in Car-2(0) mice. Normal mouse distal colon exhibited net Na(+) and Cl(-) absorption, a serosa-positive PD, and was specifically sensitive to pH. Decrease in pH stimulated active Na(+) and Cl(-) absorption whether it was caused by increasing solution PCO(2), reducing HCO(-)(3) concentration, or reducing pH in CO(2)/HCO(-)(3)-free HEPES-Ringer solution. Membrane-permeant methazolamide, but not impermeant benzolamide, at 0.1 mM prevented the effects of pH. Car-2(0) mice exhibited similar basal transport rates and responses to pH and CA inhibitors. We conclude that basal and pH-stimulated colonic electrolyte absorption in mice requires CA I. CA II and IV may have accessory roles.  (+info)

Modulation of spreading depression by changes in extracellular pH. (5/30)

Spreading depression (SD) and related phenomena have been implicated in hypoxic-ischemic injury. In such settings, SD occurs in the presence of marked extracellular acidosis. SD itself can also generate changes in extracellular pH (pH(o)), including a pronounced early alkaline shift. In a hippocampal slice model, we investigated the effect of interstitial acidosis on the generation and propagation of SD in the CA1 stratum radiatum. In addition, a carbonic anhydrase inhibitor (benzolamide) was used to decrease buffering of the alkaline shift to investigate its role in the modulation of SD. pH(o) was lowered by a decrease in saline HCO(3)(-) (from 26 to 13 to 6.5 mM at 5% CO(2)), or by an increase in the CO(2) content (from 5 to 15% in 26 mM HCO(3)(-)). Recordings with pH microelectrodes revealed respective pHo values of 7.23 +/- 0. 13, 6.95 +/- 0.10, 6.67 +/- 0.09, and 6.97 +/- 0.12. The overall effect of acidosis was an increase in the threshold for SD induction, a decrease in velocity, and a shortened SD duration. This inhibition was most pronounced at the lowest pH(o) (in 6.5 mM HCO(3)(-)) where SD was often blocked. The effects of acidosis were reversible on return to control saline. Benzolamide (10 microM) caused an approximate doubling of the early alkaline shift to an amplitude of 0.3-0.4 U pH. The amplified alkalosis was associated with an increased duration and/or increased velocity of the wave. These effects were most pronounced in acidic media (13 mM HCO(3)(-)/5% CO(2)) where benzolamide increased the SD duration by 55 +/- 32%. The initial velocity (including time for induction) and propagation velocity (measured between distal electrodes) were enhanced by 35 +/- 25 and 26 +/- 16%, respectively. Measurements of [Ca(2+)](o) demonstrated an increase in duration of the Ca(2+) transient when the alkaline shift was amplified by benzolamide. The augmentation of SD caused by benzolamide was blocked in media containing the N-methyl-D-aspartate (NMDA) receptor antagonist DL-2-amino-5-phosphonovaleric acid. These data indicate that the induction and propagation of SD is inhibited by a fall in baseline pH characteristic of ischemic conditions and that the early alkaline shift can remove this inhibition by relieving the proton block on NMDA receptors. Under ischemic conditions, the intrinsic alkalosis may therefore enable SD and thereby contribute to NMDA receptor-mediated injury.  (+info)

Interstitial carbonic anhydrase (CA) activity in brain is attributable to membrane-bound CA type IV. (6/30)

We tested the hypothesis that extracellular membrane-bound carbonic anhydrase (CA) type IV is responsible for the regulation of interstitial pH (pH(o)) transients in brain. Rat hippocampal slices were incubated in phosphatidylinositol-specific phospholipase C (PI-PLC), which cleaves the link of CA IV to the external face of plasma membranes. Then evoked alkaline pH(o) shifts were studied in a recording chamber, using pH microelectrodes. Incubation fluid was saved for later analysis. The ability to buffer a rapid alkaline load was reduced markedly in PI-PLC-treated tissue as compared with adjacent, paired control slices. The effect of benzolamide (a poorly permeant CA inhibitor) on evoked pH(o) shifts was diminished greatly in the PI-PLC-treated tissue, consistent with the washout of interstitial CA. Treatment of the incubation fluid with SDS abolished nearly all of the CA activity in fluid from controls, whereas an SDS-insensitive component remained in the fluid from PI-PLC-treated slices. These data suggested that CA type II (which is blocked by SDS) leaked from injured glial cells in both slice preparations, whereas CA type IV (which is insensitive to SDS) was liberated selectively into the fluid from PI-PLC-treated tissue. Western blot analysis was consistent with this interpretation, demonstrating a predominance of CA IV in the incubation fluid from PI-PLC-treated tissue and variable amounts of CA II in fluid from PI-PLC-treated and control slices. These results demonstrate that interstitial CA activity brain is attributable principally to membrane-bound CA IV.  (+info)

Extracellular carbonic anhydrase activity facilitates lactic acid transport in rat skeletal muscle fibres. (7/30)

1. In skeletal muscle an extracellular sarcolemmal carbonic anhydrase (CA) has been demonstrated. We speculate that this CA accelerates the interstitial CO2/HCO3- buffer system so that H+ ions can be rapidly delivered or buffered in the interstitial fluid. Because > 80 % of the lactate which crosses the sarcolemmal membrane is transported by the H+-lactate cotransporter, we examined the contributions of extracellular and intracellular CA to lactic acid transport, using ion-selective microelectrodes for measurements of intracellular pH (pHi) and fibre surface pH (pHs) in rat extensor digitorum longus (EDL) and soleus fibres. 2. Muscle fibres were exposed to 20 mM sodium lactate in the absence and presence of the CA inhibitors benzolamide (BZ), acetazolamide (AZ), chlorzolamide (CZ) and ethoxzolamide (EZ). The initial slopes (dpHs/dt, dpHi/dt) and the amplitudes (DeltapHs, DeltapHi) of pH changes were quantified. From dpHi/dt, DeltapHi and the total buffer factor (BFtot) the lactate fluxes (mM min-1) and intracellular lactate concentrations ([lactate]i) were estimated. 3. BFtot was obtained as the sum of the non-HCO3- buffer factor (BFnon-HCO3) and the HCO3- buffer factor (BFHCO3). BFnon-HCO3 was 35 +/- 4 mM pH-1 for the EDL (n = 14) and 86 /- 16 mM pH-1 for the soleus (n = 14). 4. In soleus, 10 mM cinnamate inhibited lactate influx by 44 % and efflux by 30 %; in EDL, it inhibited lactate influx by 37 % and efflux by 20 %. Cinnamate decreased [lactate]i, in soleus by 36 % and in EDL by 45 %. In soleus, 1 mM DIDS reduced lactate influx by 18 % and efflux by 16 %. In EDL, DIDS lowered the influx by 27 % but had almost no effect on efflux. DIDS reduced [lactate]i by 20 % in soleus and by 26 % in EDL. 5. BZ (0.01 mM) and AZ (0.1 mM), which inhibit only the extracellular sarcolemmal CA, led to a significant increase in dpHs/dt and pHs by about 40 %-150 % in soleus and EDL. BZ and AZ inhibited the influx and efflux of lactate by 25 %-50 % and reduced [lactate]i by about 40 %. The membrane-permeable CA inhibitors CZ (0.5 mM) and EZ (0.1 mM), which inhibit the extracellular as well as the intracellular CAs, exerted no greater effects than the poorly permeable inhibitors BZ and AZ did. 6. In soleus, 10 mM cinnamate inhibited the lactate influx by 47 %. Addition of 0.01 mM BZ led to a further inhibition by only 10 %. BZ alone reduced the influx by 37 %. 7. BZ (0.01 mM) had no influence on the Km value of the lactate transport, but led to a decrease in maximal transport rate (Vmax). In EDL, BZ reduced Vmax by 50 % and in soleus by about 25 %. 8. We conclude that the extracellular sarcolemmal CA plays an important role in lactic acid transport, while internal CA has no effect, a difference most likely attributable to the high internal vs. low extracellular BF(non-HCO3). The fact that the effects of cinnamate and BZ are not additive indicates that the two inhibitors act at distinct sites on the same transport pathway for lactic acid.  (+info)

Hemodynamics of early tubuloglomerular feedback resetting during reduced proximal reabsorption. (8/30)

BACKGROUND: Carbonic anhydrase inhibition with benzolamide reduces proximal reabsorption and activates tubuloglomerular feedback (TGF). In rats, TGF activation for 30 to 60 minutes locally suppresses renin secretion and resets TGF rightward to accommodate increased late proximal flow. After 24 hours of TGF activation, there is upward resetting of GFR and increased activity of macula densa nitric oxide synthase I (NOS I). METHODS: We studied renal hemodynamics during early TGF resetting with attention to the importance of renin suppression and NOS I activation. Left kidney blood flow (RBF, pulse Doppler) and glomerular filtration rate (GFR; inulin clearance or Fick method) were measured before and during benzolamide infusion (5 mg/kg bolus followed by 5 mg/kg/h IV) in Wistar rats concurrently receiving the converting enzyme inhibitor, enalaprilat (0.3 mg/kg/h IV) or NOS-I blocker S-methyl-thiocitrulline (SMTC; 2.7 mg/kg/h IV). RESULTS: Activating TGF initially reduced RBF and GFR in all groups as expected. During continuous benzolamide, RBF gradually increased toward baseline in control and enalaprilat-treated rats, but not in NOS I-blocked rats. After the initial decline, GFR did not change further during one hour of benzolamide in any group. CONCLUSIONS: During one hour of persistent TGF stimulation, RBF increases toward normal, but GFR does not. This requires an overall decrease in renal vascular resistance and a decrease in the ratio of efferent/afferent arteriolar resistance (RE/RA), implying a major decrease in RE. NOS I, but not angiotensin-converting enzyme (ACE), is required for RBF to increase during TGF resetting. Although the hemodynamic changes during TGF resetting resemble the response to blocking the renin-angiotensin system, these data fail to show that the increase in RBF during early TGF resetting is mediated by renin suppression.  (+info)

Background: Carbonic anhydrase is found in the blood of all vertebrate and thus playing a fundamental role in the maintenance of acid-base homeostasis. Erythrocytes are intrinsically prone to oxidative stress because of their exposure to high oxygen tension. Aim: The study aimed to investigate the changes of erythrocytes anti-oxidative enzymes in STZ induced diabetic rats and to determine the antioxidant potential of Cadaba farinosa leaves. Results: The result of the present study showed that inhibition of carbonic anhydrase result in significant decrease in both erythrocyte and plasma catalase activity, whereas erythrocyte and plasma superoxide dismutase activity increased. Conclusion: Carbonic anhydrase inhibition may alter the activity of anti-oxidative enzymes in vivo ...
Background: Carbonic anhydrase is found in the blood of all vertebrate and thus playing a fundamental role in the maintenance of acid-base homeostasis. Erythrocytes are intrinsically prone to oxidative stress because of their exposure to high oxygen tension. Aim: The study aimed to investigate the changes of erythrocytes anti-oxidative enzymes in STZ induced diabetic rats and to determine the antioxidant potential of Cadaba farinosa leaves. Results: The result of the present study showed that inhibition of carbonic anhydrase result in significant decrease in both erythrocyte and plasma catalase activity, whereas erythrocyte and plasma superoxide dismutase activity increased. Conclusion: Carbonic anhydrase inhibition may alter the activity of anti-oxidative enzymes in vivo ...
This is a short term open, randomized cross over trial to explore and compare the efficacy of pharmacological carbonic anhydrase (CA) inhibition on obstructive sleep apnea (OSA) related hypertension. Patients will be randomized to receive Acetazolamide(Diamox®)(ACZ), Continuous Positive Airway Pressure (CPAP)or CPAP plus ACZ for 2 weeks. Following a 2 week wash-out period all study participants will receive the alternative treatment regimen. The total length of the study will be 10 weeks. The effects of carbonic anhydrase inhibition on blood pressure,hemodynamics and sleep apnea will be investigated.. Study hypothesis:. Carbonic anhydrase inhibition alone or in combination with nCPAP will prominently reduce blood pressure in patients with OSA. Further it is hypothesized that CA inhibition will induce a direct pharmacological effects on vascular stiffness as evidenced in overnight non-invasive assessments of vascular stiffness and that this effect will be particularly strong in patients also ...
TY - JOUR. T1 - Carbonic anhydrase inhibition selectively prevents amyloid β neurovascular mitochondrial toxicity. AU - Solesio, María E.. AU - Peixoto, Pablo M.. AU - Debure, Ludovic. AU - Madamba, Stephen M.. AU - de Leon, Mony J.. AU - Wisniewski, Thomas. AU - Pavlov, Evgeny. AU - Fossati, Silvia. PY - 2018/8/1. Y1 - 2018/8/1. N2 - Mounting evidence suggests that mitochondrial dysfunction plays a causal role in the etiology and progression of Alzheimers disease (AD). We recently showed that the carbonic anhydrase inhibitor (CAI) methazolamide (MTZ) prevents amyloid β (Aβ)-mediated onset of apoptosis in the mouse brain. In this study, we used MTZ and, for the first time, the analog CAI acetazolamide (ATZ) in neuronal and cerebral vascular cells challenged with Aβ, to clarify their protective effects and mitochondrial molecular mechanism of action. The CAIs selectively inhibited mitochondrial dysfunction pathways induced by Aβ, without affecting metabolic function. ATZ was effective at ...
The Enterobacteriaceae vial is a membrane vial, monitoring a change in color due to a pH shift as Enterobacteriaceae organisms ferment.
The inhibition of a newly cloned human carbonic anhydrase (CA, EC 4.2.1.1), isozyme VII (hCA VII), has been investigated with a series of aromatic and heterocyclic sulfonamides, including some of the clinically used derivatives (acetazolamide, methazolamide, ethoxzolamide, dichlorophenamide, dorzolamide, brinzolamide and benzolamide), as well as the sulfamate antiepileptic drug topiramate. Inhibition data for the the other physiologically relevant cytosolic isoforms hCA I, hCA II and mCA XIII are also provided for comparison. hCA VII shows a high catalytic activity for the CO(2) hydration reaction, with a k(cat) of 9.5 x 10(5)s(-1) and k(cat)/K(m) of 8.3 x 10(7)M(-1)s(-1) at pH7.5 and 20 degrees C. A very interesting inhibition profile against hCA VII with this series of 32 sulfonamides/sulfamates was observed. hCA VII shows high affinity for all the investigated compounds, with inhibition constants in the range of 0.45-210 nM. Topiramate, ethoxzolamide and benzolamide showed subnanomolar hCA ...
Looking for Carbonic anhydrase iv? Find out information about Carbonic anhydrase iv. An enzyme which aids carbon dioxide transport and release by catalyzing the synthesis, and the dehydration, of carbonic acid from, and to, carbon dioxide... Explanation of Carbonic anhydrase iv
This study focused on the synthesis and characterization of hydrazide ligands and their respective Pd(II) complexes and used high throughput screening to determine their α-glucosidase and carbonic anhydrase II enzyme inhibition activities. The physical, analytical (elemental analyses for C, H, N and Pd) and spectral (FT-IR, 1H NMR, 13C NMR, EI-mass) techniques utilized during characterization revealed the formation of square planar, neutral and 1:2 Pd(II)-hydrazide complexes with the general formula [PdL2Cl2]. In these Pd(II) complexes, the hydrazide ligands are monodentate; the terminal nitrogen is the donor atom. The uncoordinated hydrazide ligands were inactive against both α-glucosidase and carbonic anhydrase II enzymes; however, the respective Pd(II)-hydrazide complexes were approximately 300 times more potent α-glucosidase inhibitors than the standard compound, 1-deoxynojirimycin (DNJ). Some of the Pd(II) complexes also demonstrated potential carbonic anhydrase (CA) inhibition ...
Methazolamide is a potent inhibitor of carbonic anhydrase.. Methazolamide is well absorbed from the gastrointestinal tract. Peak plasma concentrations are observed 1 to 2 hours after dosing. In a multiple-dose, pharmacokinetic study, administration of methazolamide 25 mg b.i.d., 50 mg b.i.d. and 100 mg b.i.d. demonstrated a linear relationship between plasma methazolamide levels and methazolamide dose. Peak plasma concentrations (Cmax) for the 25 mg, 50 mg and 100 mg b.i.d. regimens were 2.5 mcg/mL, 5.1 mcg/mL and 10.7 mcg/mL, respectively. The area under the plasma concentration-time curves (AUC) were 1130 mcg. min/mL, 2571 mcg. min/mL and 5418 mcg. min/mL for the 25 mg, 50 mg and 100 mg dosage regimens, respectively.. Methazolamide is distributed throughout the body including the plasma, cerebrospinal fluid, aqueous humor of the eye, red blood cells, bile and extracellular fluid. The mean apparent volume of distribution (Varea/F) ranges from 17 to 23 L. Approximately 55% is bound to plasma ...
TY - JOUR. T1 - Acetazolamide treatment prevents in vitro endotoxin-stimulated tumor necrosis factor release in mouse macrophages. AU - West, Michael A.. AU - Lemieur, Timothy L.. AU - Hackam, David. AU - Bellingham, Janet. AU - Claire, Laurel. AU - Rodriguez, Jorge L.. PY - 1998/12. Y1 - 1998/12. N2 - We previously showed that incubation in carbon dioxide (CO2), but not air or helium (He), markedly decreased macrophage intracellular pH (pHi) and resulted in reversible inhibition of lipopolysaccharide- (LPS) stimulated tumor necrosis factor (TNF) and interleukin-1 release. We sought to determine whether carbonic anhydrase inhibition with acetazolamide would prevent CO2-mediated inhibition of LPS-stimulated TNF release. Murine peritoneal macrophages were treated with acetazolamide for 1 h under control atmosphere (95% air/5% CO2) and then switched to incubator modules containing: 1) 80% CO2/20% O2, 2) 80% He/20% O2, or 3) 100% air. Before transfer to experimental atmospheric conditions the ...
TY - JOUR. T1 - Guanidinoethane sulfate. T2 - Brain pH alkaline shifter. AU - Nakada, T.. AU - Kwee, Ingrid. PY - 1993. Y1 - 1993. N2 - A new category of agents, brain pH alkaline shifters, is described. Using the prototype agent, guanidinoethane sulfate (GES), the actual alkaline shift in pH was demonstrated in adult mice brain by 31-phosphorus (31P) nuclear magnetic resonance (NMR) in vivo spectroscopy. This alkaline shift was also shown to effectively reduce the extent of brain intracellular lactic acidosis brought about by anoxic insult. These findings support the notion that a pH alkaline shift may protect the brain against the deleterious effects of lactic acidosis. Since higher pH has been shown to significantly reduce beta-amyloid deposition, alkaline shifters may also have therapeutic potential in Alzheimers disease.. AB - A new category of agents, brain pH alkaline shifters, is described. Using the prototype agent, guanidinoethane sulfate (GES), the actual alkaline shift in pH was ...
Rabbit polyclonal Carbonic Anhydrase IV/CA4 antibody validated for WB, ELISA and tested in Human and Mouse. Immunogen corresponding to synthetic peptide
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Methazolamide (Generic: Neptazane) was approved by the FDA on August 28, 1996 and is manufactured by Wyeth-Ayerst. Methazolamide is prescribed to treat glaucoma, certain kinds of tremors, and mountain or altitude sickness. Methazolamide is a carbonic anhydrase inhibitor. Carbonic anhydrase is a protein in the body, and Methazolamide reduces its activity. In treating glaucoma, Methazolamide reduces the actions of carbonic anhydrase and the amount of fluid produced in the eyes, which also reduces pressure.. There have been instances of people taking Methazolamide developing Stevens Johnson Syndrome (SJS), a rare skin disease. Stevens Johnson Syndrome can cause rash, skin peeling, and sores on the mucous membranes. Stevens Johnson Syndrome is an immune-complex mediated hypersensitivity disorder that may be caused by many drugs, viral infections, and malignancies. SJS patients are often treated in burn centers due to their open wounds and risk of infection. SJS can be fatal. Many drugs that cause ...
Effect of Hyperglycemia on Erythrocyte Carbonic Anhydrase and Lactic Acid in Type II Diabetic Subjects. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
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Many factors have been identified to contribute to the risk of ADA formation. Origin of the protein, therapy design, patients genetic background, type of disease, impurities and contamination of formulated drug may increase the risk of ADA. However, an increasing number of reports stresses the importance of protein aggregates as the major risk factor leading to ADA production. Protein aggregates have been shown to increase the immunogenicity of many therapeutic proteins like growth factors, interferons alpha and beta, insulin and monoclonal antibodies. However, not all types of aggregates are equally immunogenic. For example, it was shown that aggregates of a monoclonal antibody obtained by oxidation were more immunogenic than those obtained by shaking or pH shift. The reason for those differences remains poorly understood. One of the possible explanations is the different biodistribution of aggregated protein, as distinct stress methods lead to formation of aggregates with different ...
We have recently shown that CA IV expression in kidney cortex increased five-fold at the mRNA level (35) and 3- to 5-fold at the protein level (25) during postnatal maturation. A previous study showed a 19-fold increase in CA IV mRNA expression in rat lung between fetal day 20 and postnatal day 6, and a 40% postnatal increase to day 17, with no further increase (7). The postnatal increase was nearly comparable to what we have observed in rabbit lung (Fig. 5B). However, the increase in CA IV mRNA in kidney cortex is at least 10-fold and likely to account for the postnatal increment in protein (24). With most of the increase occurring during postnatal weeks 3-5, it is likely that the increase reflects the change in eating habits and a shift to an alkaline ash diet that requires a renal adaptation in transport. The large increase in CA IV may allow the kidney to handle the maturational increase in filtered load of bicarbonate and its proximal reabsorption.. Detailed studies of CA IX expression ...
Perrigo Company today announced that it has launched, through a distribution and supply agreement, methazolamide tablets, the generic equivalent to Neptazane tablets. This product is a component of the contingent rights Perrigo received in connection with its acquisition of a portfolio of ophthalmic products from Fera Pharmaceuticals, LLC and its affiliates in June of last year.
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Glomb-Reinmund, Sallie, and Margaret Kielian. "fus-1, a pH Shift Mutant of Semliki Forest Virus, Acts by Altering Spike Subunit Interactions via a Mutation in the E2 Subunit." Journal of Virology 72.5 (1998): 4281-4287. Web. 02 June. 2020. ...
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Learn about the potential side effects of acetazolamide. Includes common and rare side effects information for consumers and healthcare professionals.
Compare carbonic anhydrase inhibitor anticonvulsants. View important safety information, ratings, user reviews, popularity and more...
Right from the start, I want to emphasize that I am not recommending treatment or making diagnoses in this post. I am asking for information. People...
2AW1: Carbonic anhydrase inhibitors: Valdecoxib binds to a different active site region of the human isoform II as compared to the structurally related cyclooxygenase II
Looking for online definition of carbonic anhydrase inhibitor d's in the Medical Dictionary? carbonic anhydrase inhibitor d's explanation free. What is carbonic anhydrase inhibitor d's? Meaning of carbonic anhydrase inhibitor d's medical term. What does carbonic anhydrase inhibitor d's mean?
Acetazolamide-mediated decrease in strong ion difference accounts for the correction of metabolic alkalosis in critically ill patients : Metabolic alkalosis is a commonly encountered acid-base derangement in the intensive care unit. Treatment with the carbonic anhydrase inhibitor acetazolamide is indicated in selected cases. According to the quantitative approach described by Stewart, correction of serum pH due to carbonic anhydrase inhibition in the proximal tubule cannot be explained by excretion of bicarbonate. Using the
Carbonic anhydrases are abundant in mammalian tissues, plants and bacteria. The several distinct classes of this enzyme (α, β, γ etc.) share little similarity in terms of structure and sequence, but they all perform the same function of catalyzing the hydration of carbon dioxide and the dehydration of bicarbonate [3]. Carbonic anhydrase B is one of the two major forms of carbonic anhydrase in human red blood cell (the other form is CA C). Like other members of the CA family, its main function is assisting the important chemical reaction that occurs in the blood. CO2 + H2O ,-----, HCO3- + H+. The above reaction is very slow in the absence of the enzyme. Hence, by assisting the inter-conversion between carbon dioxide and bicarbonate, Carbonic anhydrase B helps to maintain acid-base balance in blood, and transport carbon dioxide out of blood. Note that the carbonic acid (H2CO3) and hydrogen carbonate ions (HCO3-) is an important buffer system in the body. They equilibrate in the blood plasma to ...
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2h15: Carbonic anhydrase inhibitors: clash with Ala65 as a means for designing inhibitors with low affinity for the ubiquitous isozyme II, exemplified by the crystal structure of the topiramate sulfamide analogue.
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Signed-off-by: Andrew Wong ,[email protected], --- builtin/reset.c , 7 ++++++- 1 file changed, 6 insertions(+), 1 deletion(-) diff --git a/builtin/reset.c b/builtin/reset.c index 6004803..740263d 100644 --- a/builtin/reset.c +++ b/builtin/reset.c @@ -318,7 +318,12 @@ int cmd_reset(int argc, const char **argv, const char *prefix) _(reset_type_names[reset_type])); } if (reset_type == NONE) - reset_type = MIXED; /* by default */ + { + if(is_merge()) + reset_type = MERGE; + else + reset_type = MIXED; + } if (reset_type != SOFT && reset_type != MIXED) setup_work_tree(); -- 1.9.0.6.g16e5f9a -- To unsubscribe from this list: send the line unsubscribe git in the body of a message to [email protected] More majordomo info at http://vger.kernel.org/majordomo-info.html ...
Mentos brand mints cause the carbonation in soda to very rapidly come out of solution. You can find plenty of photos and videos of it online, and Ive...
In vertebrates, carbonic anhydrases (CAs) play important roles in ion transport and pH regulation in many organs, including the eyes, kidneys, central nervous system, and inner ear. In aquatic organis
18.05.2017 · Hyperkalemia is defined as a serum potassium concentration higher than the upper limit of the normal range; the range in
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Carbonic Anhydrase Inhibitors (Acetazolamide and Azopt) are often used to decrease IOP in conditions such as hyphema or glaucoma. However, in Sickle Cell disease, they can increase sickling secondary to hemoconcentration and systemic acidosis. If you must choose a CAI for a patient with SCD, then use Methazolamide which is less likely to cause problems ...
1. Cyclic AMP-stimulated protein kinase activity phosphorylating intrinsic substrates in preparations of synaptic-membrane fragments from ox cerebral cortex was examined in relation to (a) the content of membrane-bound Ca2+in the preparations and (b) added Ca2+in the assay medium. 2. Centrifugal washing of synaptic-membrane fragments with buffered ethane dioxybis(ethylamine)tetra-acetate solutions decreased bound Ca2+from 2.8±0.4 (s.d.) to 0.9±0.3nmol/mg of protein. In washed preparations basal protein kinase activity was increased by about 40% and the cyclic AMP-stimulated activity by about 15%. Addition of Ca2+in the concentration range 5-50μm to the assay medium progressively inhibited the kinase activity of the washed preparations; in this range of Ca2+concentration the basal activity was inhibited more than the stimulated activity. 3. In unwashed preparations concentrations of Ca2+above 100μm inhibited the cyclic AMP-stimulated activity more than the basal activity. 4. The inhibitory ...
Coumarins were recently shown to constitute a novel class of mechanism-based carbonic anhydrase (CA, EC 4.2.1.1) inhibitors. We demonstrate that sulfocoumarins (1,2-benzoxathiine 2,2-dioxides) possess a similar mechanism of action, acting as effective CA inhibitors. The sulfocoumarins were hydrolyzed by the esterase CA activity to 2-hydroxyphenyl-vinylsulfonic acids, which thereafter bind to the enzyme in a region rarely occupied by other classes of inhibitors. The X-ray structure of one of these compounds in adduct with a modified CA II enzyme possessing two amino acid residues from the CA IX active site, allowed us to decipher the inhibition mechanism. The sulfonic acid was observed anchored to the zinc-coordinated water molecule, making favorable interactions with Thr200 and Pro201. Some other sulfocoumarins incorporating substituted-1,2,3-triazole moieties were prepared by using click chemistry and showed low nanomolar inhibitory action against the tumor-associated isoforms CA IX and XII, ...
Wang, Xiaolong and Maroto-Valer, Mercedes Dissolution kinetics of minerals for advanced mineral carbonation. In: 7th European Conference on Coal Research & its Application, 3-5 Sept 2008, Cardiff, UK. (Unpublished) ...
Definition of acetazolamide in the Legal Dictionary - by Free online English dictionary and encyclopedia. What is acetazolamide? Meaning of acetazolamide as a legal term. What does acetazolamide mean in law?
Kjøp Acetazolamide 250mg uten resept online i Norge, Sverige, Danmark, Tyskland og andre europeiske land. Rask levering over hele Europa.
The IUPHAR/BPS Guide to Pharmacology. acetazolamide ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
Though carcinoids are slow growing tumors, which can be treated by surgery, the survival in metastatic carcinoids is very low because the treatment strategies for other cancers are not effective for dealing with advanced stage carcinoids [36]. Therefore, the investigations concerning the discovery of new strategies for treating pulmonary carcinoids need to be focused on therapies that can inhibit the growth and invasiveness of advanced stage disease. Carcinoid tumors are proving moderately responsive to newer therapies targeting tumor vasculature and survival pathways [1, 2]. The mammalian target of rapamycin (mTOR) inhibitor, everolimus, has shown promising initial results alone or combined with other agents [37-39]. Bronchial AC, which is characterized by high mTOR expression, has been reported to be responders to mTOR inhibition, indicating that therapies targeting the critical survival pathways are potential candidates to treat bronchial carcinoids [40]. The evidence seems to indicate that ...
Trithiocarbonate (CS32-) inhibits with low micromolar affinities several mammalian carbonic anhydrases, CAs, EC 4.2.1.1 [Innocenti et al., Bioorg. Med. Chem. Lett. 2009, 19, 1855]. Here we report the X-ray crystal structure of the hCA II-trithiocarbonate adduct. Trithiocarbonate is monodentately bound to the Zn(II) ion and makes several hydrogen bonds with Thr199 and two water molecules from the enzyme active site. Its binding is different from that of ureate, another small inhibitor isosteric with trithiocarbonate but somehow mimicks the binding of the SO(2)NH moiety present in the sulfonamide inhibitors and is similar to that of bicarbonate. Compounds incorporating this new zinc-binding group, CS2-, may thus lead to new classes of potent inhibitors. Carbonic anhydrase inhibitors. X-ray crystal studies of the carbonic anhydrase II-trithiocarbonate adduct--an inhibitor mimicking the sulfonamide and urea binding to the enzyme.,Temperini C, Scozzafava A, Supuran CT Bioorg Med Chem Lett. 2010 Jan ...
Acetazolamide is a carbonic anhydrase inhibitor used to treat symptoms of altitude sickness. It also belongs to the class of diuretics and it is effective in the treatment of glaucoma, epileptic attacks, intracranial hypertension, cystinuria, dural ectasia. | Ph24h.com
Zonisamide is a sulfonamide anticonvulsant and a carbonic anhydrase inhibitor indicated as adjunctive therapy in the treatment of partial seizures in adults with epilepsy.
The presence of chloride ions is one of the primary factors causing the degradation of reinforced concrete structures. An investigation to monitor ingress of chlorides during a 24-week wetting and drying exposure regime to simulate conditions in which multiple-mode transport mechanisms are active was conducted on a variety of binders. Penetration was evaluated using free and total chloride profiles. Acid extraction of chlorides is quantitatively reliable and practical for assessing penetration. X-ray diffraction was used to determine the presence of bound chlorides and carbonation. The ability of the cement blends to resist chloride penetration was, from best to worst, ground granulated blast-furnace slag, microsilica, pulverised-fuel ash, Portland cement. The effect of carbonation on binding capability was observed and the relative quantity of chlorides also showed a correlation with the amount of chlorides bound in the form of Friedels salt.
In health, Your whole body fluid tonicity is regulated by ADH and thirst. These mechanisms function very perfectly. In overall health, Your whole body fluid volume is regulated generally by atrial natriuretic peptide, thats created when the right atrium feels that extra extend, and which mediates a number of consequences. Considering the fact that body fluid tonicity is so well-controlled, extracellular system fluid quantity is actually a measure of overall system sodium. This mechanism will work pretty much. In wellness, your full overall body potassium is regulated primarily by diffusion of potassium out of your near percentage of the distal convoluted tubule in reaction to intracellular pH shifts, which consequently mirror your potassium load. This mechanism wont get the job done extremely perfectly ...
ACETAZOLAMIDE INJECTION (Acetazolamide) drug information & product resources from MPR including dosage information, educational materials, & patient assistance.
Learn about Diamox Sequels (Acetazolamide XR) may treat, uses, dosage, side effects, drug interactions, warnings, patient labeling, reviews, and related medications.
... benzolamide MeSH D03.383.129.708.867.537 --- methazolamide MeSH D03.383.129.708.867.768 --- timolol MeSH D03.383.129.708.900 ...
... benzolamide MeSH D02.886.675.867.537 --- methazolamide MeSH D02.886.675.867.768 --- timolol MeSH D02.886.675.900 --- thiamine ... benzolamide MeSH D02.065.884.150 --- bumetanide MeSH D02.065.884.344 --- chloramines MeSH D02.065.884.365 --- chlorthalidone ... benzolamide MeSH D02.886.590.700.135 --- benzothiadiazines MeSH D02.886.590.700.135.138 --- bendroflumethiazide MeSH D02.886. ...
benzolamide ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs. ...
Hastening respiratory acclimatization to altitude with benzolamide (CL 11,366). Aerospace Med1967;39:296-300. ...
Sulfonamide drugs (known widely as "sulfa drugs") were the first antimicrobial drugs, and paved the way for the antibiotic revolution in medicine. The first sulfonamide was trade named Prontosil, which is a prodrug. Experiments with Prontosil began in 1932 in the laboratories of Bayer AG, at that time a component of the huge German chemical trust IG Farben. The dye-based drug was synthesized by Bayer chemist Josef Klarer and tested in animals under the direction of physician/researcher Gerhard Domagk. Domagk quickly won the 1939 Nobel Prize in Medicine and Physiology, an honor that Adolf Hitler forbade him to accept (Hitler was incensed at the awarding of a Nobel Peace Prize a few years earlier to an anti-Nazi activist). Domagks prize also caused some bad feeling between him and Klarer. The discovery was in fact a team effort in which Domagk played a central role, operating under the general direction of Heinrich Hoerlein, a Farben executive later tried (and acquitted) at Nuremberg. The first ...
... after benzolamide administration, P less than 0.01. Benzolamide had no effect on chloride reabsorption in the distal convoluted ... For comparison, another group of rats was studied before and after 2 mg/kg per h benzolamide, a carbonic anhydrase inhibitor. ... by benzolamide administration, P less than 0.001. The increased delivery very of chloride from the proximal tubule was largely ... but did not change after benzolamide. The influence of chlorothiazide on proximal chloride transport presumably is related to ...
Membrane-impermeable CA inhibitors (benzolamide and pd5000) did not have this effect. Addition of CA II antisense ...
Benzolamide is a highly potent drug used to inhibit various carbonic anhydrase isoforms with a concentration for half-maximal ... A few experiments were performed with bath-applied atropine (5 μm) or eserine (5-10 μm). Benzolamide (BA), a poorly permeant ... Second, there was no suppression of the GDPSP after internal perfusion of the pyramidal neuron with benzolamide. These results ... First, inhibition of interstitial carbonic anhydrase by bath-applied benzolamide did not suppress the GDPSP. ...
Benzolamide is a highly potent drug used to inhibit various carbonic anhydrase isoforms with a concentration for half-maximal ... A few experiments were performed with bath-applied atropine (5 μm) or eserine (5-10 μm). Benzolamide (BA), a poorly permeant ... Second, there was no suppression of the GDPSP after internal perfusion of the pyramidal neuron with benzolamide. These results ... First, inhibition of interstitial carbonic anhydrase by bath-applied benzolamide did not suppress the GDPSP. ...
... benzolamide, topiramate, and indisulam showed effective inhibitory activity (Kis of 18-62 nM). Three compounds showed better ...
... benzolamide, chlorzolamide, ethoxzolamide, and methazolamide), and compared to CA II. This structural information has been ...
... benzolamide MeSH D03.383.129.708.867.537 --- methazolamide MeSH D03.383.129.708.867.768 --- timolol MeSH D03.383.129.708.900 ...
... benzolamide MeSH D02.886.675.867.537 --- methazolamide MeSH D02.886.675.867.768 --- timolol MeSH D02.886.675.900 --- thiamine ... benzolamide MeSH D02.065.884.150 --- bumetanide MeSH D02.065.884.344 --- chloramines MeSH D02.065.884.365 --- chlorthalidone ... benzolamide MeSH D02.886.590.700.135 --- benzothiadiazines MeSH D02.886.590.700.135.138 --- bendroflumethiazide MeSH D02.886. ...
... There are several sulfonamide-based groups of drugs. The original antibacterial sulfonamides (sometimes called simply sulfa
Molitoris, B. A., Okusa, M. D., Palevsky, P. M., Chawla, L. S., Kaufman, J. S., Devarajan, P., Toto, R. M., Hsu, C. Y., Greene, T. H., Faubel, S. G., Kellum, J. A., Wald, R., Chertow, G. M., Levin, A., Waikar, S. S., Murray, P. T., Parikh, C. R., Shaw, A. D., Go, A. S., Chinchilli, V. M. & 15 others, Liu, K. D., Cheung, A. K., Weisbord, S. D., Mehta, R. L., Stokes, J. B., Thompson, A. M., Taylor Thompson, B., Westenfelder, C. S., Tumlin, J. A., Warnock, D. G., Shah, S. V., Xie, Y., Duggan, E. G., Kimmel, P. L. & Star, R. A., May 1 2012, In : Clinical Journal of the American Society of Nephrology. 7, 5, p. 856-860 5 p.. Research output: Contribution to journal › Article ...
... benzolamide, chlorzolamide, ethoxzolamide, and methazolamide), and compared to CA II. This structural information has been ...
Benzolamide. -6.85. [1]. View 5. Bevantolol. -4.27. [4]. View 6. N-bromoacetazolamide. -6.42. [1]. View ...
A group of compounds that contain the structure SO2NH2. Members of this group, also known as sulfa drugs, are derivatives of sulfanilamide, which competitively inhibit folic acid synthesis in microorganisms, and are bacteriostatic. They have been largely supplanted by more effective and less toxic antibiotics. (From Dorland, 28th ed)
A sulfamoylbenzamide analog of CLOPAMIDE. It is diuretic and saluretic with antihypertensive activity. It is bound to PLASMA PROTEINS, thus has a delayed onset and prolonged action.
Serum levels of apolipoprotein altitude with benzolamide (CL for Index Divorce project. The effect of thyroid set during ...
Some CA inhibitors, such as acetazolamide and benzolamide, are less membrane-permeable than others and as such are not as ... Supuran CT, Scozzafava A. Benzolamide is not a membrane-impermeant carbonic anhydrase inhibitor. J Enzyme Inhib Med Chem. 2004; ...
Benzolamide -- Teratogenic Agent *Benztropine Mesylate -- Teratogenic Agent *Benzyl Alcohol -- Teratogenic Agent *Betamtehasone ...
Another carbonic anhydrase inhibitor, benzolamide, caused no change in systemic acid-base state but produced a decrease in ...
Topiramate, ethoxzolamide and benzolamide showed subnanomolar hCA VII inhibitory activity, whereas acetazolamide, methazolamide ... Topiramate, ethoxzolamide and benzolamide showed subnanomolar hCA VII inhibitory activity, whereas acetazolamide, methazolamide ... brinzolamide and benzolamide), as well as the sulfamate antiepileptic drug topiramate. Inhibition data for the the other ... brinzolamide and benzolamide), as well as the sulfamate antiepileptic drug topiramate. Inhibition data for the the other ...
... different effects of benzolamide and methazolamide in the anaesthetized cat", J. Physiol. (Lond), Vol. 488, (1995), pp. 767-777 ...
... benzolamide, bumetanide, chlorthalidone, clopamide, dichlorphenamide, ethoxzolamide, indapamide, mafenide, mefruside, ...
Benzolamide Complexes. *Binding Of Sugar Sulfamates To Cas. *C - 2. *C c c c c o c ...
  • L. Teppema, A. Berkenbosch, J. DeGoede and C. Olievier: "Carbonic anhydrase and the control of breathing: different effects of benzolamide and methazolamide in the anaesthetized cat", J. Physiol. (edu.pl)
  • Benzolamide had no effect on chloride reabsorption in the distal convoluted tubule. (uptodate.com)