Selective renal carbonic anhydrase inhibitor. It may also be of use in certain cases of respiratory failure.
A class of compounds that reduces the secretion of H+ ions by the proximal kidney tubule through inhibition of CARBONIC ANHYDRASES.
A carbonic anhydrase inhibitor used as diuretic and in glaucoma. It may cause hypokalemia.
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
A membrane-bound carbonic anhydrase found in lung capillaries and kidney.
A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma.
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.
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)
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.

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)

Benzolamide is not a recognized medication or pharmaceutical agent in modern medical practice. It is possible that you may have misspelled the name, and there are no direct synonyms for any known medications. If you meant to search for a different term or have more information about the context where this term was used, please let me know so I can provide a more accurate response.

Carbonic anhydrase inhibitors are a class of medications that work by blocking the action of carbonic anhydrase, an enzyme that is responsible for converting carbon dioxide and water into carbonic acid. This enzyme is found in various tissues throughout the body, including the eyes, kidneys, and nervous system.

By inhibiting the activity of carbonic anhydrase, these medications can reduce the production of bicarbonate ions in the body, which helps to lower the rate of fluid buildup in certain tissues. As a result, carbonic anhydrase inhibitors are often used to treat conditions such as glaucoma, epilepsy, and altitude sickness.

In glaucoma, for example, these medications can help to reduce pressure within the eye by promoting the drainage of fluid from the eye. In epilepsy, carbonic anhydrase inhibitors can help to reduce the frequency and severity of seizures by reducing the acidity of the blood and brain. And in altitude sickness, these medications can help to alleviate symptoms such as headache, nausea, and shortness of breath by reducing the buildup of fluid in the lungs.

Some common examples of carbonic anhydrase inhibitors include acetazolamide, methazolamide, and dorzolamide. These medications are available in various forms, including tablets, capsules, and eye drops, and are typically prescribed by a healthcare professional.

Ethoxzolamide is a carbonic anhydrase inhibitor drug that is primarily used to reduce fluid buildup in the eye (ocular pressure) caused by glaucoma or other conditions. It works by decreasing the production of fluid inside the eye, which helps lower the pressure within the eye.

Ethoxzolamide may also be used for other medical purposes, such as treating seizure disorders and preventing altitude sickness. The drug is available in oral tablet form and is typically taken 2-3 times a day.

It's important to note that Ethoxzolamide can have side effects, including frequent urination, tingling sensations in the hands or feet, loss of appetite, and changes in taste perception. It may also interact with other medications, so it's essential to inform your healthcare provider about all the drugs you are taking before starting Ethoxzolamide therapy.

Carbonic anhydrases (CAs) are a group of enzymes that catalyze the reversible reaction between carbon dioxide and water to form carbonic acid, which then quickly dissociates into bicarbonate and a proton. This reaction is crucial for maintaining pH balance and regulating various physiological processes in the body, including respiration, secretion of electrolytes, and bone resorption.

There are several isoforms of carbonic anhydrases found in different tissues and organelles, each with distinct functions and properties. For example, CA I and II are primarily found in red blood cells, while CA III is present in various tissues such as the kidney, lung, and eye. CA IV is a membrane-bound enzyme that plays a role in transporting ions across cell membranes.

Carbonic anhydrases have been targeted for therapeutic interventions in several diseases, including glaucoma, epilepsy, and cancer. Inhibitors of carbonic anhydrases can reduce the production of bicarbonate and lower the pH of tumor cells, which may help to slow down their growth and proliferation. However, these inhibitors can also have side effects such as kidney stones and metabolic acidosis, so they must be used with caution.

Carbonic anhydrase IV (CA-IV), also known as membrane-associated carbonic anhydrase or CA-IX, is a member of the carbonic anhydrase enzyme family. This enzyme is responsible for catalyzing the reversible reaction that converts carbon dioxide and water into bicarbonate and a proton.

CA-IV is primarily found in the plasma membrane of polarized epithelial cells, where it plays a crucial role in maintaining acid-base balance and ion transport. It is also involved in various physiological processes, including respiration, bone resorption, and pH regulation.

Abnormalities in CA-IV expression or activity have been implicated in several diseases, such as cancer, kidney stones, and osteoporosis. In particular, overexpression of CA-IV has been observed in various types of cancer, where it contributes to tumor acidification, invasion, and metastasis. Therefore, CA-IV is considered a potential therapeutic target for cancer treatment.

Methazolamide is a sulfonamide-derived carbonic anhydrase inhibitor primarily used in the prevention and treatment of glaucoma. It works by decreasing the production of fluid inside the eye, which in turn lowers the pressure within the eye. Additionally, it has been used off-label for conditions such as altitude sickness, epilepsy, intracranial hypertension, and benign prostatic hyperplasia.

The medical definition of Methazolamide is:
A carbonic anhydrase inhibitor that reduces the secretion of aqueous humor, thereby lowering intraocular pressure; used in the treatment of glaucoma. It also has diuretic properties and has been used in the management of altitude sickness, epilepsy, intracranial hypertension, and benign prostatic hyperplasia.

Bicarbonates, also known as sodium bicarbonate or baking soda, is a chemical compound with the formula NaHCO3. In the context of medical definitions, bicarbonates refer to the bicarbonate ion (HCO3-), which is an important buffer in the body that helps maintain normal pH levels in blood and other bodily fluids.

The balance of bicarbonate and carbonic acid in the body helps regulate the acidity or alkalinity of the blood, a condition known as pH balance. Bicarbonates are produced by the body and are also found in some foods and drinking water. They work to neutralize excess acid in the body and help maintain the normal pH range of 7.35 to 7.45.

In medical testing, bicarbonate levels may be measured as part of an electrolyte panel or as a component of arterial blood gas (ABG) analysis. Low bicarbonate levels can indicate metabolic acidosis, while high levels can indicate metabolic alkalosis. Both conditions can have serious consequences if not treated promptly and appropriately.

Acetazolamide is a medication that belongs to a class of drugs called carbonic anhydrase inhibitors. It works by decreasing the production of bicarbonate in the body, which helps to reduce the amount of fluid in the eye and brain, making it useful for treating conditions such as glaucoma and epilepsy.

In medical terms, acetazolamide can be defined as: "A carbonic anhydrase inhibitor that is used to treat glaucoma, epilepsy, altitude sickness, and other conditions. It works by decreasing the production of bicarbonate in the body, which helps to reduce the amount of fluid in the eye and brain."

Acetazolamide may also be used for other purposes not listed here, so it is important to consult with a healthcare provider for specific medical advice.

Kidney tubules are the structural and functional units of the kidney responsible for reabsorption, secretion, and excretion of various substances. They are part of the nephron, which is the basic unit of the kidney's filtration and reabsorption process.

There are three main types of kidney tubules:

1. Proximal tubule: This is the initial segment of the kidney tubule that receives the filtrate from the glomerulus. It is responsible for reabsorbing approximately 65% of the filtrate, including water, glucose, amino acids, and electrolytes.
2. Loop of Henle: This U-shaped segment of the tubule consists of a thin descending limb, a thin ascending limb, and a thick ascending limb. The loop of Henle helps to concentrate urine by creating an osmotic gradient that allows water to be reabsorbed in the collecting ducts.
3. Distal tubule: This is the final segment of the kidney tubule before it empties into the collecting duct. It is responsible for fine-tuning the concentration of electrolytes and pH balance in the urine by selectively reabsorbing or secreting substances such as sodium, potassium, chloride, and hydrogen ions.

Overall, kidney tubules play a critical role in maintaining fluid and electrolyte balance, regulating acid-base balance, and removing waste products from the body.

DuBose, T. D. ; Seldin, D. W. ; Pucacco, L. R. / Effect of I.V. benzolamide on proximal tubular pH and pCO2. In: Kidney ... Effect of I.V. benzolamide on proximal tubular pH and pCO2. / DuBose, T. D.; Seldin, D. W.; Pucacco, L. R. In: Kidney ... DuBose, T. D., Seldin, D. W., & Pucacco, L. R. (1978). Effect of I.V. benzolamide on proximal tubular pH and pCO2. Kidney ... DuBose, TD, Seldin, DW & Pucacco, LR 1978, Effect of I.V. benzolamide on proximal tubular pH and pCO2, Kidney international, ...
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 MeSH D03.383.129.708.867.537 - methazolamide MeSH D03.383.129.708.867.768 - timolol MeSH D03.383.129.708.900 - ...
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Benzolamide 11,366 From 1963-66. *Benzolamide and related topics-Strassbarg Data. *Subacute Toxicity Study with a Benzolamide- ...
Benzolamide [D02.886.590.700.120] * Benzothiadiazines [D02.886.590.700.135] * Bosentan [D02.886.590.700.143] ...
... while the membrane permeant CAI benzolamide (10-3 M) fully dilated all arteriolar segments tested. This suggests that CAI act ...
Benzolamide [D02.886.590.700.120] Benzolamide * Benzothiadiazines [D02.886.590.700.135] Benzothiadiazines * Bosentan [D02.886. ...
Benzolamide [D02.886.590.700.120] Benzolamide * Benzothiadiazines [D02.886.590.700.135] Benzothiadiazines * Bosentan [D02.886. ...
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