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At least 19 recordsLinked to original sources
PubMed1996

Cerebral blood flow alteration by acetazolamide during carotid balloon occlusion: parameters reflecting cerebral perfusion pressure in the acetazolamide test.

BACKGROUND AND PURPOSE: We attempted to clarify the role of the acetazolamide-reactive mechanism in cerebral hemodynamic autoregulation and to establish a useful method of estimation using the acetazolamide test. METHODS: We examined 18 patients whose cerebral hemodynamics were considered to be normal and whose cerebral blood flow (CBF) was maintained during the balloon occlusion test (BOT) of the internal carotid artery. We measured the mean stump pressure (MSTP) and the mean CBF in the middle cerebral arterial territory using a xenon-enhanced CT system during BOT with and without acetazolamide activation. We obtained the asymmetry ratio (AR=occluded CBF/contralateral CBF) and the increased CBF parameters caused by acetazolamide activation expressed as an absolute value (delta CBF) and a percentage (%delta CBF) for the occluded side. RESULTS: AR during BOT with and without acetazolamide activation differed significantly (P<.001, paired t test) despite the lack of significant MSTP changes. Furthermore, although there was no significant correlation between MSTP and AR without acetazolamide activation, a positive significant correlation was detected with acetazolamide activation (r=.634, P=.005, linear regression analysis). There were significant correlations between delta CBF and MSTP (r=.574, P=.013) and %delta CBF and MSTP (r=.640, P=.004). CONCLUSIONS: We consider that the acetazolamide-reactive mechanism functions as autoregulation at the lower end of the autoregulatory range. The acetazolamide test, using %delta CBF or delta CBF as parameters (which both directly reflect MSTP), is useful for estimating the cerebral perfusion pressure decrease and presence of hemodynamic compromise.

Acetazolamide↗
PubMed2006

Acetazolamide 125 mg BD is not significantly different from 375 mg BD in the prevention of acute mountain sickness: the prophylactic acetazolamide dosage comparison for efficacy (PACE) trial.

750 mg per day of acetazolamide in the prevention of acute mountain sickness (AMS), as recommended in the meta-analysis published in 2000 in the British Medical Journal, may be excessive and is controversial. To determine if the efficacy of low-dose acetazolamide 125 mg bd (250 mg), as currently used in the Himalayas, is significantly different from 375 mg bd (750 mg) of acetazolamide in the prevention of AMS, we designed a prospective, double-blind, randomized, placebo-controlled trial. The participants were sampled from a diverse population of (non-Nepali) trekkers at Namche Bazaar (3440 m) in Nepal on the Everest trekking route as they ascended to study midpoints (4280 m/4358 m) and the endpoint, Lobuje (4928 m), where data were collected. Participants were randomly assigned to receive 375 mg bd of acetazolamide (82 participants), 125 mg bd of acetazolamide (74 participants), or a placebo (66 participants), beginning at 3440 m for up to 6 days as they ascended to 4928 m. The results revealed that composite AMS incidence for 125 mg bd was similar to the incidence for 375 mg bd (24% vs. 21%, 95% confidence interval, -12.6%, 19.8%), in contrast to significantly greater AMS (51%) observed in the placebo group (95% confidence interval for differences: 8%, 46%; 12%, 49% for low and high comparisons, respectively). Both doses of acetazolamide improved oxygenation equally (82.9% for 250 mg daily and 82.8% for 750 mg daily), while placebo endpoint oxygen saturation was significantly less at 80.7% (95% confidence interval for differences: 0.5%, 3.9% and 0.4%, 3.7% for low and high comparisons, respectively). There was also more paresthesia in the 375-mg bd group (p < 0.02). We conclude that 125 mg bd of acetazolamide is not significantly different from 375 mg bd in the prevention of AMS; 125 mg bd should be considered the preferred dosage when indicated for persons ascending to altitudes above 2500 m.

Acetazolamide↗
PubMed1998

Acetazolamide plus low-dose dexamethasone is better than acetazolamide alone to ameliorate symptoms of acute mountain sickness.

METHODS: In a double-blind study, we compared the efficacy of a combination of sustained-release acetazolamide and low-dose dexamethasone and acetazolamide alone for prophylaxis against acute mountain sickness (AMS) caused by rapid ascent to high altitude. Before ascent, 13 subjects were randomly assigned to receive a combination of one sustained-release acetazolamide capsule (500 mg) in the afternoon and 4 mg dexamethasone every 12 h, or a combination of the same dose of acetazolamide once daily and a placebo every 12 h. Days 1 and 2 were spent at 3698 m (La Paz, Bolivia), while days 3 and 4 were spent at 5334 m (Mount Chaclataya, Bolivia). Ascent was by 2 h motor vehicle ride. Heart rates, peripheral oxygen saturations and a modified score derived from the Environmental Symptom Questionnaire (modified-ESQ) were measured on each day. In addition, weighted averages of the cerebral (AMS-C) and respiratory (AMS-R) symptoms were calculated for days 3 and 4. RESULTS: Heart rate and modified-ESQ scores increased on days 3 and 4 compared with the other days in the acetazolamide/placebo group only (p < 0.05). Oxygen saturations decreased in both groups on days 3 and 4 (p < 0.05), but the decrease was greater in the acetazolamide/placebo group (p < 0.05). AMS-C and AMS-R scores rose above the suggested thresholds for indication of AMS on days 3 and 4 in the acetazolamide/placebo group only (p < 0.05). CONCLUSION: We conclude that this combination of sustained-release acetazolamide once daily and low-dose dexamethasone twice daily is more effective in ameliorating the symptoms of AMS than azetazolamide alone at the ascent that was studied.

Acetazolamide↗
PubMed1984

Dissociation of glucose and potassium arterial-venous differences across the forearm by acetazolamide. A possible relationship to acetazolamide's beneficial effect in hypokalemic periodic paralysis.

We studied the effect of acetazolamide on arterial-venous (A-V) glucose and potassium differences across the forearm following oral glucose loading in eight normal subjects. Administration of acetazolamide for 72 hours prior to glucose loading resulted in increased A-V glucose differences and decreased A-V potassium differences. Acetazolamide may, therefore, increase glucose uptake across muscle while decreasing potassium uptake following glucose ingestion. This glucose-potassium dissociation observed in normal subjects may relate to acetazolamide's beneficial effect in hypokalemic periodic paralysis.

Acetazolamide↗
PubMed2004

Clinical significance of cerebrovascular reserve in acetazolamide challenge -comparison with acetazolamide challenge H2O-PET and Gas-PET.

OBJECTIVE: The response of cerebral blood flow (CBF) to acetazolamide (ACZ) challenge is frequently determined in clinical settings to evaluate cerebrovascular reserve (CVR). A reduced CVR can indicate patients with occlusive cerebrovascular disease and compromised hemodynamics who may be at increased risk of cerebral ischemia. However, how precisely ACZ reflects cerebral hemodynamic impairment remains obscure. The present study aims to clarify the pathological significance of CVR in patients with occluded carotid arteries. METHODS: We recruited seventeen patients with occlusive lesions in the internal carotid artery (ICA) or middle cerebral artery (MCA). We assessed these patients in terms of resting cerebral blood flow (CBF) and the CVR response to ACZ challenge using H20 positron emission tomography (PET). In addition, we evaluated hemodynamic parameters including oxygen extraction fraction (OEF) using Gas-PET. RESULTS: We identified a significant negative correlation between the CVR and OEF or the cerebral blood volume (CBV)/CBF ratio, as a potential index of cerebral perfusion pressure. Although the CVR values were reduced in all regions with elevated OEF (Stage II), these values were highly variable regardless of the CBV/CBF ratios. The cut-off value of CVR alone could not detect Stage II, but when combined with resting CBF, misery perfusion accompanied by increased OEF was detected with high sensitivity (6/7) and specificity (61/62). CONCLUSION: CVR could be applied as an index reflecting both autoregulatory capacity and OEF. The present study also supported the notion that SPECT with ACZ challenge can be clinically applied to detect misery perfusion.

Acetazolamide↗
PubMed1982

Effect of exogenous adenosine 3':5'-cyclic monophosphate, parathyroid hormone and acetazolamide on electrolyte hormone and acetazolamide on electrolyte excretion by the isolated perfused rat kidney.

The effects of exogenous adenosine 3':5'-cyclic monophosphate (cyclic AMP), parathyroid hormone (PTH) and acetazolamide (Az) on renal calcium and phosphate excretion of the isolated perfused rat kidney were compared. Both PTH and Az evoked an early increase in urinary cyclic AMP excretion followed by a later more prolonged increase in phosphate excretion. All of the increased urinary cyclic AMP was derived from renal cells. Calcium excretion decreased with PTH but was unchanged with Az. Sodium and potassium excretion increased with Az but not PTH. Transitory urinary cyclic AMP excretion rates following bolus additions of exogenous cyclic AMP to perfusate were up to twentyfold greater than those evoked by PTH or Az but unassociated with changes in calcium, phosphate, sodium or potassium excretion. Sustained perfusate levels (above 0.5 microM) and excretion rates of cyclic AMP induced phosphaturia proportional to the perfusate cyclic AMP concentrations achieved up to 2.0 microM. Clearances of exogenous cyclic AMP exceeded inulin clearance at perfusate concentrations greater than 1.0 microM. Aminophylline evoked a small phosphaturia which increased further on addition of cyclic AMP to 5 microM. Glomerular filtration was not affected by any of the agents except Az. Since increased phosphate excretion could be evoked only at perfusate concentrations exceeding either plasma or intracellular concentrations observed in vivo, it is concluded that circulating cyclic AMP at levels in vivo is unlikely to mediate a significant fraction of the renal effects of PTH.

Acetazolamide↗
PubMed2004

[Effect of acetazolamide on the latency of hyperbaric oxygen-induced convulsion].

The purpose of the present study was to explore the relation between the modulation of cerebral blood flow and the latency of hyperbaric oxygen-induced convulsion. There were two parts in this study. First, the effect of acetazolamide on the latency of hyperbaric oxygen-induced convulsion was observed. 32 Sprague-Dawley (SD) rats were randomly divided into four groups: the acetazolamide 200, 20, 2 mg/kg body weight and normal saline (NS) group. The animals were given intraperitoneally acetazolamide or NS, respectively, before being exposed to the pressure of 6 ATA (absolute atmosphere) of pure oxygen. The time from exposure to the onset of seizure (clonic-tonic convulsion) was recorded for each animal according to behavioral observation. Second, the changes in maleic dialdehyde (MDA) and the activity of glutathione peroxidase (GSH-PX) were measured after acetazolamide treatment. 40 SD rats were randomly divided into five groups: NS group, 6 min with NS group, 6 min with acetazolamide group, 16 min with NS group, and 16 min with acetazolamide group. The dose of acetazolamide was 20 mg/kg body weight. After injection of NS or acetazolamide, the animals were subjected to the pressure of 6 ATA of pure oxygen in respect to its time course group. The rats were decapitated and the cortex, hippocampus, and striatum of brains were dissected and homogenized. The content of MDA and the activity of GSH-PX in these tissues were determined. We found that (1) there was a significant difference in the latency of hyperbaric oxygen-induced convulsion between the acetazolamide 200 mg/kg group and the NS control group, as well as between the acetazolamide 20 mg/kg group and the NS control group (P<0.01), whereas there was no significant difference between the NS group and the acetazolamide 2 mg/kg weight group (P>0.05). The latency of these groups were listed as follows: 9.78+/-1.94 min for 200 mg/kg body weight group, 10.92+/-1.68 min for 20 mg/kg body weight group, 24.32+/-4.33 min for 2 mg/kg body weight group and 22.02+/-4.32 min for NS control group. (2) there was no significant difference between all groups in the activity of GSH-PX, though it varied with the oxidation levels. In the cortex and hippocampus, the activity of GSH-PX boosted up at first, but with the progress of the oxidation it was impaired. In the striatum, the activity of GSH-PX increased stepwise with the aggravation of the oxidation. The MDA content in the cortex increased significantly in the group of 6 min with acetazolamide (P<0.01), as well as the group of 16 min with acetazolamide group both in cortex and hippocampus (P<0.01, P<0.05). The MDA content of all groups is correlated with the dose of acetazolamide and the exposure time. These results suggest that acetazolamide which dilates the brain arteriolar obviously shortens the latency of hyperbaric oxygen-induced convulsion, and that acetazolamide dilates the vessels and increases the supply of the oxygen breaking into the brain tissues and aggravates the oxidation. The hyperbaric oxygen-induced convulsion correlates closely with the oxidation injury.

Acetazolamide↗
PubMed1996

Growth suppression in children receiving acetazolamide with antiepileptic drugs.

To clarify the effect of the clinical dosage of acetazolamide on growth in children with epilepsy or febrile convulsion, the standard scores of height and weight in 17 subjects receiving acetazolamide as an adjunct to unchanged monotherapy of antiepileptic drug were compared longitudinally through four phases: before antiepileptic drug administration, with monotherapy of antiepileptic drug, with acetazolamide in addition to monotherapy, and after acetazolamide discontinuation. The standard scores of both height and weight in the subjects were significantly reduced during the phase of acetazolamide administration. During this period, serum concentrations of potassium and total CO2 decreased while that of chloride increased, suggesting the existence of metabolic acidosis in the subjects. For both height and weight, there was no correlation between the degree of standard score reduction during acetazolamide administration and age at the time of acetazolamide initiation, duration of acetazolamide administration, dosages of acetazolamide, and variety of antiepileptic drugs concomitantly administered with acetazolamide. We speculate that metabolic acidosis induced by acetazolamide suppressed the growth of the subjects and that there were large individual differences in the susceptibility to acetazolamide for growth suppression among patients receiving acetazolamide.

Acetazolamide↗
PubMed2006

Effect of acetazolamide on leg endurance exercise at sea level and simulated altitude.

Acetazolamide can be taken at sea level to prevent acute mountain sickness during subsequent altitude exposure. Acetazolamide causes metabolic acidosis at sea level and altitude, and increases SaO2 (arterial oxygen saturation) at altitude. The aim of the present study was to determine whether acetazolamide impairs muscle endurance at sea level but not simulated altitude (4300 m for <3 h). Six subjects (20+/-1 years of age; mean+/-S.E.M.) performed exhaustive constant work rate one-leg knee-extension exercise (25+/-2 W) once a week for 4 weeks, twice at sea level and twice at altitude. Each week, subjects took either acetazolamide (250 mg) or placebo orally in a double-blind fashion (three times a day) for 2 days. On day 2, all exercise bouts began approx. 2.5 h after the last dose of acetazolamide or placebo. Acetazolamide caused similar acidosis (pH) in all subjects at sea level (7.43+/-0.01 with placebo compared with 7.34+/-0.01 with acetazolamide; P<0.05) and altitude (7.48+/-0.03 with placebo compared with 7.37+/-0.01 with acetazolamide; P<0.05). However, endurance performance was impaired with acetazolamide only at sea level (48+/-4 min with placebo compared with 36+/-5 min with acetazolamide; P<0.05), but not altitude (17+/-2 min with placebo compared with 20+/-3 min with acetazolamide; P = not significant). In conclusion, lack of impairment of endurance performance by acetazolamide compared with placebo at altitude was probably due to off-setting secondary effects resulting from acidosis, e.g. ventilatory induced increase in SaO2 for acetazolamide compared with placebo (89+/-1 compared with 86+/-1% respectively; P<0.05), which resulted in an increased oxygen pressure gradient from capillary to exercising muscle.

Acetazolamide↗
PubMed2005

[Influence of acetazolamide given intraperitoneally on the latency to hyperbaric oxygen-induced convulsion of rats.].

The purpose of the present study was to explore the relation between the modulation of cerebral blood flow and the latency of hyperbaric oxygen-induced convulsion. There were two parts in this study. First, the effect of acetazolamide or (and) indomethacin on the latency of hyperbaric oxygen-induced convulsion was observed. Seventy Sprague-Dawley (SD) rats were randomly divided into 7 groups: the acetazolamide 200, 20, 10, 7.5, 5, 2.5 mg/kg body weight and normal saline (NS) group. Forty rats were divided into 5 groups: indomethacin 20, 10, 5, 2.5 mg/kg body weight and NS groups. Another 40 rats were divided into 5 groups which were administered with indomethacin in the dose of 0 mg/kg (NS), 0 mg/kg (NS), 5, 10 and 20 mg/kg body weight. Thirty min later the first group was given NS, and all the other four groups were given acetazolamide with a dose of 7.5 mg/kg body weight. The animals were given acetazolamide or (and) indomethacin intraperitoneally, and 20 min later they were exposed to the pressure of 6 ATA (absolute atmosphere) of pure oxygen. The time from exposure to the onset of seizure (clonic-tonic convulsion) was recorded for each animal according to behavioral observation. Second, the change of maleic dialdehyde (MDA) was measured after acetazolamide and (or) indomethacin treatment. Seventy-two SD rats were randomly divided into 9 groups: Control, 6 and 16 min respectively with NS, acetazolamide, indomethacin, and both acetazolamide and indomethacin group. The dose of acetazolamide was 7.5 mg/kg body weight and the dose of indomethacin was 20 mg/kg body weight. After injection of drugs, the animals were subjected to the pressure of 6 ATA of pure oxygen in respect to its time course group. Then the rats were decapitated and the cerebral cortex was dissected and homogenized. The content of MDA was determined. We found that (1) when the dose of acetazolamide is higher than 7.5 mg/kg, it shortened the latency to hyperbaric oxygen-induced convulsion significantly (P<0.05, P<0.01). There was no significant difference in the latency between every to hyperbaric oxygen-induced convulsion significantly (P<0.05, P<0.01). There was no significant difference in the latency between every two groups of rats treated with different doses of indomethacin. But when the rats were administered acetazolamide of 7.5 mg/kg body weight after being pretreated with indomethacin of 20 mg/kg body weight, the outbreak of convulsion was put off remarkably (P<0.05). (2) In comparison with the control, the content of MDA in the group treated with acetazolamide increased significantly (P<0.01), but when the rats were treated with both acetazolamide and indomethacin, the content of MDA was reduced significantly both in 6 and 16 min exposure time projects (P<0.05, P<0.01). These results suggest that acetazolamide which dilates the brain arterioles can obviously shorten the latency of hyperbaric oxygen-induced convulsion and aggravate the oxidation of the brain. Indomethacin can resist acetazolamideos effect on the latency and oxidation level when the animals were exposed to the hyperbaric oxygen. The activity of carbonic anhydrase correlates closely with the oxidation injury.

English Abstract↗
PubMed1987

Role of carbonic anhydrase in bone resorption: effect of acetazolamide on basal and parathyroid hormone-induced bone metabolism.

The effects of the carbonic anhydrase inhibitor acetazolamide on basal and parathyroid hormone (PTH)-induced bone metabolism were studied to evaluate the manner in which acetazolamide inhibits bone resorption. Half-calvaria from 5 to 6-day-old mice were cultured using the following treatments: control; acetazolamide (10, 33, or 100 microM); PTH (16.7 nM bovine PTH 1-34); acetazolamide + PTH. The effects of acetazolamide on PTH-induced cAMP accumulation and protein synthesis were determined. Media from bones cultured for 48 hours were analyzed for calcium to assess bone resorption, glucose to assess calvarial glucose utilization, and lactic acid to assess calvarial lactic acid release. Media were also assayed for beta-glucuronidase activity as an indicator of lysosomal enzyme release and for lactate dehydrogenase activity as an indicator of cytosolic enzyme release and cytotoxicity. Acetazolamide at 100 microM completely inhibited PTH-induced bone resorption. This inhibition did not appear to be due to cell death, as acetazolamide did not increase lactate dehydrogenase release. Acetazolamide had no effect on PTH-enhanced cAMP levels, indicating that receptor binding and adenylate cyclase activation were unaffected. Acetazolamide alone did not alter calvarial protein synthesis, but did significantly inhibit protein synthesis in the presence of PTH. PTH significantly enhanced calvarial glucose utilization, lactic acid release, and beta-glucuronidase release. Acetazolamide inhibited all of these PTH-induced parameters in a manner that roughly paralleled its inhibition of bone resorption; acetazolamide alone had no effect on the basal values. Our results indicate that acetazolamide inhibition of bone resorption in vitro may involve general alterations in hormonally stimulated bone cell metabolism secondary to carbonic anhydrase inhibition.

Acetazolamide↗
PubMed1986

Toxic interaction between acetazolamide and salicylate: case reports and a pharmacokinetic explanation.

Two elderly patients, who were chronically receiving aspirin, developed lethargy, incontinence, and confusion after dosing with acetazolamide. Unbound plasma acetazolamide concentrations were elevated and plasma protein binding was reduced, suggesting an interaction with aspirin. In vitro studies demonstrated a concentration-dependent effect of salicylate on acetazolamide binding to serum proteins. At a therapeutic serum acetazolamide level of 8.0 micrograms/ml, the unbound percentage of acetazolamide in serum was 3.3% and increased to 11.0% and 30.0%, with serum salicylate levels of 200 and 386 micrograms/ml, respectively. Furthermore, the apparent association constant of acetazolamide for binding to serum proteins was decreased by 58% and 86% of its control value at these respective salicylate concentrations. The maximal binding capacity of serum for acetazolamide was not affected by salicylate. Pharmacokinetic studies in four volunteers showed that the plasma protein binding and renal clearance of acetazolamide were significantly reduced during chronic salicylate dosing. Salicylate appears to competitively inhibit the plasma protein binding of acetazolamide and simultaneously to inhibit acetazolamide renal tubular secretion. Caution is advised when acetazolamide and salicylate are used concurrently.

Acetazolamide↗
PubMed2002

Tolerability and efficacy of dorzolamide versus acetazolamide added to timolol.

PURPOSE: Evaluate the safety and efficacy of dorzolamide versus acetazolamide when added to once daily 0.5% timolol maleate ophthalmic gel forming solution (timolol gel). METHODS: This was a randomized, double-masked, multicenter, active-controlled, parallel group study of 215 patients with open-angle glaucoma or ocular hypertension. Following a two-week treatment period with timolol gel, patients with IOP > or = 22 mm Hg and who tolerated one week of acetazolamide 250-mg q.i.d. either were randomized to acetazolamide or dorzolamide 2% three times daily for 12 weeks. RESULTS: In 155 randomized patients (dorzolamide, N = 80, acetazolamide, N = 75), compared to the dorzolamide, acetazolamide had a statistically greater number of systemic adverse events (dorzolamide 50%, acetazolamide 75%, p = 0.001), adverse events associated with carbonic anhydrase inhibitor (CAI) therapy (dorzolamide 26%, acetazolamide 53%, p < 0.001) and discontinuations due to CAI adverse experiences (dorzolamide 8%, acetazolamide 24%, p = 0.007). Intent to treat analysis found that changes from baseline in IOP were similar at both troughs (dorzolamide 1.4 +/- 0.46 mm Hg, acetazolamide 0.8 +/- 0.47 mm Hg, p = 0.386). However, per-protocol analysis found statistically improved pressure control with acetazolamide (0.1 +/- 0.42 mm Hg) compared to dorzolamide (1.9 +/- 0.43 mm Hg) (p = 0.009). CONCLUSIONS: This study found a greater incidence of systemic and CAI adverse experiences and discontinuations due to acetazolamide compared to dorzolamide.

Acetazolamide↗
PubMed1995

Time dependency of the acetazolamide effect on cerebral hemodynamics in patients with chronic occlusive cerebral arteries. Early steal phenomenon demonstrated by [15O]H2O positron emission tomography.

BACKGROUND AND PURPOSE: The acetazolamide effect is thought to reach a maximum at 10 to 20 minutes after administration. However, we sometimes encountered patients who showed a transient deterioration of ischemic symptoms several minutes after acetazolamide administration. We therefore considered that a steal phenomenon may occur before the acetazolamide effect reaches a maximum. We evaluated the time dependency of the acetazolamide effect on cerebral hemodynamics in patients with severe stenosis or occlusion of the unilateral internal carotid artery. METHODS: The subjects consisted of 13 patients with severe stenosis or occlusion of the unilateral internal carotid artery. Regional cerebral blood flow was measured at the resting state and at 5 and 20 minutes after the intravenous administration of 1 g acetazolamide by the use of the [15O]H2O bolus-injection method and positron emission tomography. The steal phenomenon was interpreted as positive when the regional cerebral blood flow values decreased by more than 10% after the administration of acetazolamide in more than one region of interest. RESULTS: A steal phenomenon was observed in 5 of 13 patients at 5 minutes after acetazolamide administration on the occlusive side, whereas it was observed in only 1 patient at 20 minutes. Thus, this phenomenon was observed more frequently in the early phase of the acetazolamide test. It was also observed more frequently in patients with poorly developed collateral circulation. CONCLUSIONS: Our acetazolamide [15O]H2O positron emission tomography study revealed an early steal phenomenon at 5 minutes after intravenous administration of acetazolamide, which may be a cause of the transient deterioration of ischemic symptoms during the acetazolamide test.

Acetazolamide↗
PubMed1989

Effects of acetazolamide on Na+-HCO-3 cotransport in basolateral membrane vesicles isolated from rabbit renal cortex.

We evaluated the effects of acetazolamide on Na+-HCO3- cotransport in basolateral membrane vesicles isolated from the rabbit renal cortex. Na+ uptake stimulated by an imposed inward HCO3- gradient was not significantly reduced by 1.2 mM acetazolamide, indicating that acetazolamide does not directly inhibit Na+-HCO3- cotransport. 4,4'-Diisothiocyanostilbene-2,2'-disulfonate (DIDS)-sensitive Na+-base cotransport was found to be absolutely CO2/HCO3--dependent. We therefore tested whether acetazolamide-sensitive availability of HCO3- at the basolateral membrane could be rate-limiting for Na+-base cotransport under some conditions. In the presence of a CO2/HCO3- buffer system but absence of an initial HCO3- gradient, Na+ influx was stimulated fivefold by an outward NH4+ gradient. This stimulation of Na+ influx by an outward NH4+ gradient was inhibited greater than 75% by 0.6 mM acetazolamide, suggesting that acetazolamide blocked the ability of the NH4+ gradient to generate an inward HCO3- gradient. In the presence of an inward HCO3- gradient, Na+ influx was inhibited greater than 70% by an inward NH4+ gradient. This inhibition of Na+ influx was reduced to only 35% by 0.6 mM acetazolamide, suggesting that acetazolamide blocked the ability of NH4+ to collapse the inward HCO3- gradient. Similarly, Na+ influx in the presence of an inward HCO3- gradient was inhibited greater than 80% by an outward acetate gradient, and this inhibition was reduced to only 50% by acetazolamide. Thus, acetazolamide caused either inhibition or stimulation of Na+ uptake depending on the conditions with respect to pH and HCO3- gradients. The indirect interaction of acetazolamide with the basolateral membrane Na+-HCO3- cotransport system may be an important mechanism underlying inhibition of proximal tubule acid secretion by this agent.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗