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PubMed1979

Carbonic anhydrase-dependent bicarbonate reabsorption in the rat proximal tubule.

The extent to which bicarbonate reabsorption in the rat proximal convoluted tubule depends on carbonic anhydrase has been examined by in vivo microperfusion and the measurement of total CO2 concentration by microcalorimetry. Tubules were perfused with an ultrafiltrate-like solution at 13 nl/min, and volume reabsorptive rate (JV) was measured using [14C]inulin. Addition of either 800 or 100 microM acetazolamide to the perfusion solution completely inhibited the reabsorption of total CO2. The control total CO2 reabsorptive rate (JtCO2) was 147 +/- 23 pmol/mm.min, and acetazolamide reduced JtCO2 to -3 +/- 5 pmol/mm.min. Acetazolamide reduced JV by 65% from a control of 2.3 +/- 0.4 to 0.8 +/- 0.1 nl/mm.min. The dose-response curve for acetazolamide showed that the I50 for inhibition of JtCO2 was 4 microM. The inactive congener of acetazolamide, t-butyl acetazolamide, did not reduce JV or inhibit bicarbonate reabsorption, indicating that the effect of acetazolamide on JtCO2 was specific for carbonic anhydrase inhibition. Since bicarbonate reabsorption was completely blocked by carbonic anhydrase inhibition, there is no need to postulate either carbonic acid recycling or carbonic anhydrase-independent bicarbonate reabsorption.

Acetazolamide↗
PubMed2002

Quantitative measurement of regional cerebral blood flow with flow-sensitive alternating inversion recovery imaging: comparison with [iodine 123]-iodoamphetamin single photon emission CT.

BACKGROUND AND PURPOSE: Flow-sensitive alternating inversion recovery (FAIR) MR imaging is a technique for depicting cerebral perfusion without contrast enhancement. Our purpose was to determine whether quantification at FAIR imaging can be used to assess regional cerebral blood flow (rCBF) in a manner similar to [iodine 123]-iodoamphetamin ((123)I-IMP) single photon emission CT (SPECT). METHODS: Nine patients with internal carotid or major cerebral arterial stenosis underwent (123)I-IMP SPECT and FAIR imaging (single section, different TIs, 1.5 T) at rest and after acetazolamide (Diamox) stress. FAIR and (123)I-IMP rCBF values were compared and correlated. Receiver operating characteristic analysis was conducted to detect hypoperfused segments on FAIR images. RESULTS: rCBF values of normally perfused segments were 41.53 and 51.91 mL/100 g/min for pre- and post-acetazolamide (123)I-IMP studies, respectively. Corresponding values for pre- and post-acetazolamide FAIR images, respectively, were 46.64 and 59.60 mL/100 g/min with a TI of 1200 milliseconds and 53.23 and 68.17 mL/100 g/min with a TI of 1400 milliseconds. (123)I-IMP and FAIR results were significantly correlated, with both pre- and post-acetazolamide images. Sensitivity (86%) in detecting hypoperfused segments was significantly higher with post-acetazolamide images (TI, 1400 milliseconds), and specificity (82-85%) and accuracy (80-82%) were higher with all pre- and post-acetazolamide images (all TIs). CONCLUSIONS: The significant correlation, high specificity and accuracy in detecting hypoperfused segments, similar increases in flow on both post-acetazolamide images, and absence of the need for contrast enhancement suggest that FAIR imaging, like nuclear medicine study, is complementary to routine MR imaging in the assessment of cerebral perfusion.

Acetazolamide↗
PubMed1976

Pharmacological characterization of lithium reabsorption in the rat.

The effects of furosemide, chlorothiazide and acetazolamide upon fractional lithium excretion (FELi) were studied in acutely lithium-loaded rats. Changes in FELi were compared with the fractional excretions of sodium FENa and calcium FECa. Furosemide and acetazolamide, given separately, produced large and substantially equivalent increases in FELi. Responses of FENa and FECa to acetazolamide were much less than to furosemide. Chlorothiazide, alone or in combination with the other agents, produced moderate increases in FENa, modest increases in FECa and essentially no change in FELi. When furosemide was superimposed upon a previously established acetazolamide diuresis, the response in FELi was additive to that from acetazolamide alone. These results suggest that lithium reabsorption occurs at nephron sites primarily affected by acetazolamide and furosemide in the rat and that a significant amount of lithium reabsorption may take place in the loop of Henle. Acetazolamide, in combination with furosemide, appeared to depress renal tissue lithium accumulation.

Absorption↗
PubMed2004

[Nitric oxide and carbon dioxide in neurotoxicity induced by oxygen under pressure].

Hyperbaric oxygen (HBO2) causes CO2 retention in the brain that leads to the increase in cerebral blood flow (CBF) by poorly understood mechanisms. We have tested the hypothesis that NO is implicated in CBF-responses to hypercapnia under hyperoxic conditions. Alert rats were exposed to HBO2 at 5 ata and blood flow in the striatum measured by H2 clearance every 10 min. Acetazolamide, the inhibitor of carbonic anhydrase, was used to increase brain PCO2. CBF responses to acetazolamide administration (30 mg/kg, i.p.) were assessed in rats breathing air at 1 ata or oxygen at 5 ata with and without NOS inhibition (L-NAME, 30 mg/kg, i.p.). In rats breathing air, acetazolamide increased CBF by 34 +/- 7.4% over 30 min and by 28 +/- 12% over 3 hours while NOS inhibition with L-NAME attenuated acetazolamide-induced cerebral vasodilatation. HBO2 at 5 ata reduced CBF during the first 30 min hyperoxia, after that CBF increased by 55 +/- 19% above pre-exposure levels. In acetazolamide-treated animals, no HBO, induced vasoconstricton was observed and striatal blood flow increased by 53 +/- 18% within 10 min of hyperbaric exposure. After NOS inhibition, cerebral vasodilatation in response to acetazolamide during HBO2 exposure was significantly attenuated. The study demonstrates that NO is implicated in acetazolamide (CO2)-induced cerebral hyperemia under hyperbaric oxygen exposure.

Acetazolamide↗
PubMed1972

Carbonic anhydrase function and the epithelial organization of H+ secretion in turtle urinary bladder.

The function of carbonic anhydrase in H(+) secretion by the turtle bladder was studied in vitro. Dose response curves were obtained for the carbonic anhydrase inhibitors, acetazolamide and ethoxzolamide, with and without addition of CO(2) to the system. In addition, carbonic anhydrase was assayed in homogenates of mucosal cells. The activity in the homogenates was 155+/-16 U/g dry wt, of which only 11 U represented contamination from erythrocytes; after addition of 5 x 10(-6)m acetazolamide, no enzyme activity was detectable. In the intact preparation free of exogenous CO(2), the dose response curve for acetazolamide showed two plateaus of inhibition, one at 50% and one at more than 80% inhibition. At 50% inhibition (from 5 x 10(-6) to 5 x 10(-5)m acetazolamide), H(+) secretion was restored or enhanced by CO(2) addition to the same extent as bladders not exposed to acetazolamide. At concentrations of more than 1 x 10(-4)m, H(+) secretion was no longer restorable by CO(2). Unlike acetazolamide, ethoxzolamide caused progressive inhibition of H(+) secretion in the CO(2)-free system. The maximal extent of inhibition with ethoxzolamide and the behavior of inhibition in the presence of 2.5% CO(2) were the same as for acetazolamide. Evidence is presented that all surface epithelial cells secrete H(+) and generate OH(-) within the cell interior. The capacity of cells to dispose of OH(-) by CO(2) hydroxylation varies with the availability of cytoplasmic carbonic anhydrase. A small population of cells contains abundant carbonic anhydrase and secretes at high rates even when CO(2) is in short supply. On the basis of these results and histochemical data on the distribution of carbonic anhydrase within the mucosa, an analysis is presented of the epithelial organization of acidification by the turtle bladder.

Animals↗
PubMed1997

Cerebrovascular reactivity in hypertensive patients: a transcranial Doppler study.

PURPOSE: We studied the usefulness of transcranial Doppler sonography for assessing changes in vasoreactivity in patients with hypertension and the hemodynamic consequences of hypertension. METHODS: The study group comprised 25 patients with chronic severe hypertension and 25 age- and sex-matched healthy subjects. Cerebrovascular reserve capacity was assessed by transcranial Doppler recording of the blood flow velocity in both middle cerebral arteries before and 5, 10, 15, and 20 minutes after intravenous injection of 1 g of acetazolamide (Diamox). Blood pressure, blood gases, and other blood parameters were also measured before and after acetazolamide injection. The sizes of the left atrium, left ventricle, and aortic root were measured by echocardiography and correlated with the vasoreactivity after acetazolamide injection. RESULTS: After acetazolamide injection, no significant changes in blood pressure were observed in either group. The mean blood flow velocity in the middle cerebral arteries of hypertensive patients (60.8 +/- 2.6 cm/sec) was not significantly different from that of controls (58.8 +/- 1.9 cm/sec) before acetazolamide injection. Ten minutes after acetazolamide injection, the percentage change in blood flow velocity was significantly lower in the hypertensive group (36.2 +/- 4.5%) than in the controls (52.6 +/- 3.7%). A significant negative correlation (p < 0.05) between decreased vasoreactivity and increased size of the left atrium and aortic root was observed. CONCLUSIONS: Vasoreactivity decreases in hypertensive patients without neurologic deficits or computed tomography abnormalities. Enlargement of the left atrium correlates well with the severity of the impairment in vasoreactivity. Transcranial Doppler sonography can be a sensitive tool in the investigation of vascular impairment caused by hypertension and in the follow-up of hypertensive patients.

Acetazolamide↗
PubMed2002

Quantitative assessment of blood flow reserve using 99mTc-HMPAO in carotid stenosis.

Dynamic imaging of the inflow of technetium-99m hexamethylpropylene amine oxime (HMPAO) to the brain has been proved to allow estimation of the hemispherical cerebral blood flow (CBF) using the Patlak plot. In this study, we compared the hemispherical CBF (in ml/min/100 g) of different patient groups. A total of 25 patients (comprising 13 with migraine and 12 scheduled for endarterectomy owing to angiographically confirmed severe stenosis of the internal carotid artery on at least one side) underwent baseline and acetazolamide 99mTc-HMPAO brain perfusion studies. In addition, acetazolamide 99mTc-HMPAO studies were performed in 12 healthy subjects (no baseline study was performed for ethical reasons.) Dynamic studies were acquired by means of a dual-detector gamma camera with a large field of view (HELIX, Elscint). Special difference images were created to make definition of the aortic arch and hemispherical brain regions easier and more reproducible. A semi-automatic method was developed to determine the transit time from the aorta to the brain, making the generation of the Patlak plot even more robust. The baseline CBF values did not significantly depend on the disease (P>0.1), whereas the CBF values obtained after acetazolamide provocation did do so (ANOVA, P<0.001). Patients suffering from migraine showed a significant increase in global CBF values after acetazolamide provocation (paired t test, P<0.05), but we could not find any effect of the provocation in patients awaiting carotid endarterectomy, indicating a lack of cerebrovascular reserve capacity. Comparison of the results of the acetazolamide study in patients and the control group revealed the CBF values to be significantly lower in patients with carotid stenosis (two-sample t-test, P<0.001), but not in those with migraine (P>0.1). In summary, using quantitative analysis of 99mTc-HMPAO brain studies we could objectively compare the CBF of patients suffering from different diseases. Especially the CBF values obtained after acetazolamide provocation permitted effective differentiation of disease states. The quantitative results may be of assistance in therapy planning, e.g. in selection of the correct operative technique.

Acetazolamide↗
PubMed1984

Relationship of renal prostaglandins to three diuretics.

The effects of amiloride, a potassium-sparing diuretic, and of acetazolamide, a carbonic anhydrase inhibitor, were compared to those of triamterene, a potent prostaglandin stimulator which may result in acute renal failure after indomethacin pretreatment. Eighteen normal subjects on a constant sodium diet were given triamterene 200 mg/d, or amiloride 15 mg/d, or acetazolamide 750 mg/d for 3 days. Plasma potassium rose after triamterene and amiloride, and fell after acetazolamide. Natriuresis was increased after amiloride and acetazolamide, but not after triamterene. Plasma renin activity and urinary aldosterone were stimulated by the three diuretics. Triamterene induced a 4-fold increase in urinary prostaglandins E2 and F2 alpha and acetazolamide a 2-fold increase in prostaglandin E2 only, whereas amiloride showed no effect. No relationship was found between plasma or urinary electrolytes and urinary prostaglandins. Renal function was preserved in all cases. These results which show that amiloride, unlike triamterene, does not stimulate prostaglandins, suggest that nonsteroidal anti-inflammatory drugs (NSAID) which unmask triamterene nephrotoxicity may not constitute a hazard in association with amiloride. The prostaglandin response to acetazolamide may be indicative of adverse reactions during concomitant NSAID administration.

Acetazolamide↗
PubMed1993

Dose response from pharmacological interventions for CBF changes in a baboon model using 99Tcm-HMPAO and SPECT.

This study assesses the sensitivity of the baboon model under anaesthesia to determine by single photon emission computed tomography (SPECT) and 99Tcm-hexamethylpropyleneamine oxime (HMPAO) dose responses from drugs (acetazolamide) with known regional cerebral blood flow (rCBF) effects on humans. Three dosages of acetazolamide were chosen: 250, 500 and 750 mg. The effects of these were studied by conventional SPECT 5 min after intravenous (i.v.) administration and compared to previous studies of rCBF with the baboons under anaesthesia only. An additional study concerned the effect of 500 mg acetazolamide at 15 min after administration. Haemodynamic parameters and blood gases were also monitored. No statistically significant regional effects were noted (P > 0.05). The largest increase in CBF (39%) was observed from 500 mg acetazolamide after 5 min. This was statistically significantly different from control values only at a 10% level of confidence; then followed a 27% increase above control values after 750 mg (5 min). At 15 min 500 mg yielded values lower by 10% than the high dose. No effects were observed from 250 mg acetazolamide; only pO2 showed changes which largely confirm the CBF findings. The model did not give significant results at a 5% level of confidence but large fluctuations were observed, also in the haemodynamic and blood gas values. At a 10% level a significant dose response was confirmed for acetazolamide.

Acetazolamide↗
PubMed2006

Optical coherence tomography in the diagnosis and monitoring of cystoid macular edema in patients with retinitis pigmentosa.

PURPOSE: To identify cystoid macular edema (CME) in patients with retinitis pigmentosa (RP) using optical coherence tomography (OCT) and to evaluate response to acetazolamide by serial OCT. METHODS: Twenty-nine consecutive RP patients were included in the study. Patients with CME were treated with acetazolamide (125 or 250 mg/d for 4-12 months). OCT, fluorescein angiography, and determination of best-corrected visual acuity (BCVA) were performed initially and throughout the follow-up period. RESULTS: Ten of the 29 patients had CME by OCT. Of these 10 patients, 5 had various degrees of fluorescein leakage by fluorescein angiography. After acetazolamide treatment, six patients had significant decreases in macular edema in at least one eye by follow-up OCT. In six patients, visual acuity improved by > or =1 line in at least one eye. The change of central foveal thickness shown by OCT was significantly correlated with the change of logMAR of BCVA (Pearson correlation coefficient [r] = 0.576; P = 0.008). We observed no differences in the change of central foveal thickness by OCT (Mann-Whitney test; P = 1.000) and in the change of logMAR of BCVA (Mann-Whitney test; P = 0.106) between patients treated with 125 mg/d acetazolamide and those treated with 250 mg/d acetazolamide. CONCLUSIONS: These results indicate that OCT is a valuable tool in the detection and follow-up of CME in RP patients. Treatment with acetazolamide resulted in marked improvement in OCT-diagnosed CME in RP, but visual improvement was variable.

Acetazolamide↗
PubMed1990

Is central chemoreceptor sensitive to intracellular rather than extracellular pH?

The chemosensitive area on the ventral surface of the brain stem responds to local acidosis by eliciting hyperventilation and to local alkalosis by hypoventilation. The stimulus is conventionally thought to be the hydrogen ion concentration in the area's extracellular fluid. It is pointed out, however, that the elegant studies by Loeschcke & Ahmad have demonstrated that [pH]e and [pH]i are normally tightly and rapidly coupled (Loeschcke & Ahmad, 1980). For this reason, the stimulus might just as well be the intracellular hydrogen ion concentration in the chemoreceptor area. The administration of acetazolamide allows the dissociation of [pH]e from [pH]i. With acetazolamide a sharp acid shift of CSF pH [( pH]c) is measured and in two consonance with this shift a marked increase in CBF is seen. Comparing these two reactions to that obtained with CO2 breathing, it is apparent that 7% CO2 causes about the same decrease in [pH]e and the same increase in CBF. In other words CBF acidosis can quantitatively account for the CBF increase induced by acetazolamide. But CO2 and acetazolamide influence [pH]i quite differently, as CO2 drops [pH]i to almost the same extent as [pH]c, while two recent studies by MR spectroscopy have shown that acetazolamide does not drop [pH]i measurably, if tissue hypercapnia is prevented in artificially ventilated rabbits or by the mild spontaneous hyperventilation caused by acetazolamide in normal man.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetazolamide↗
PubMed1977

Diuretics and the renal adenylate cyclase system.

1 The relationship between the diuretic effectiveness and the effect on the renal adenylate cyclase of three diuretics, acetazolamide, frusemide and ethacrynic acid, was examined. The hypothesis that acetazolamide and parathyroid hormone (PTH), inhibit renal carbonic anhydrase by a cyclic adenosine 3',5'-monophosphate (cyclic AMP)-dependent mechanism was also tested.2In vitro, acetazolamide, frusemide and ethacrynic acid at high concentrations (10(-3)M) all produced some inhibition of basal and stimulated rat kidney plasma membrane adenylate cyclase. The effect of acetazolamide was much less than that of frusemide and ethacrynic acid. These plasma membrane effects were reproduced in studies of cyclic AMP formation in isolated kidney tubules of rats.3 Intravenous injections of acetazolamide did not change the total cyclic AMP content of the kidneys of rats killed by microwave irradiation.4 Acetazolamide produced a diuresis in the rat and a slight inhibition of the antidiuretic effect of Pitressin. Frusemide produced a diuresis and greatly reduced the antidiuretic response to Pitressin. Ethacrynic acid was ineffective as a diuretic in the rat and actually enhanced the antidiuretic response to Pitressin.5 In investigating the possible influence of diuretics and PTH on the activity and state of phosphorylation of carbonic anhydrase it was found that: there was no correlation between the ability of diuretics to inhibit carbonic anhydrase activity and to inhibit carbonic anhydrase phosphorylation; neither PTH nor cyclic AMP (in the presence of adenosine triphosphate, Mg(2+), K(+) and incubation at 37 degrees C) inhibited rat cortex homogenate carbonic anhydrase activity.6 It seems unlikely that any of the tested diuretics exerts its pharmacological effect by means of changes in kidney cyclic AMP metabolism.

Acetazolamide↗
PubMed1996

Assessment of the ophthalmic artery as a collateral to the cerebral circulation. A comparison of transorbital Doppler ultrasonography and regional cerebral blood flow measurements.

The role of the ophthalmic artery (OA) as a collateral to the cerebral circulation in carotid occlusive disease is somewhat controversial. The aim of this study was to assess the importance of this collateral by comparing the results of transorbital Doppler ultrasonography and regional cerebral blood flow measurements using SPECT and Xenon-133 inhalation in 41 patients with unilateral high-grade internal carotid artery occlusive disease. Both measurements were performed under basal conditions and after the intravenous administration of 1 g acetazolamide to test cerebral vasoreactivity. Based on the direction of OA flow, the patients could be divided into three groups. In Group 1 (n = 16) with anterograde OA flow before and after acetazolamide, baseline rCBF values did not differ significantly between the two sides, or from those of the controls. The side-to-side asymmetry of the response to acetazolamide was also normal. In Group 2 (n = 11) where the OA flow was anterograde or "0 flow" before, but became retrograde after acetazolamide, rCBF was significantly reduced on the symptomatic compared to the non-symptomatic side under basal conditions. However, the increase in rCBF after acetazolamide was within normal limits. In Group 3 (n = 14) the OA flow was reversed both under basal conditions and after the vasodilatory stimulus. Baseline rCBF was significantly lower (p < 0.05) on the symptomatic side compared to the non-symptomatic, and the asymmetry became even greater (p < 0.001) after acetazolamide. Our findings demonstrate that the OA may be an important collateral pathway in patients with ICA occlusive disease, and contribute to the cerebral perfusion reserve in the case of compromised blood supply.

Acetazolamide↗
PubMed1981

Protection of the rat gastric mucosa by prostaglandin E2: possible relation to stimulation of the alkaline secretion.

Exogenous prostaglandins have specific protective effects on the gastric mucosa called cytoprotection which is proposed to be connected to the stimulatory effects of prostaglandins on the gastric nonparietal secretions. The protection by oral prostaglandin E2 (PGE2) against indomethacin-induced gastric erosions was studied in the rat, as was the effect on the protection of blocking the gastric alkaline secretion by acetazolamide. PGE2 reduced dose-dependently the indomethacin gastric erosion formation, confirming previous results from others. Acetazolamide caused very little damage when given alone but potentiated the indomethacin erosion formation in a dose-related way. PGE2 was less protective or without effect against lesions caused by indomethacin when given together with acetazolamide, but protection could be obtained by increasing the doses of PGE2. Indomethacin and acetazolamide are both blockers of the gastric bicarbonate secretion, which is stimulated by PGE2. The potentiation of indomethacin induced lesions by acetazolamide and the antagonistic actions between acetazolamide and PGE2 on mucosal protection are compatible with the hypothesis that stimulation of the alkaline secretion is one mechanism of cytoprotection of the gastric mucosa by PGE2.

Acetazolamide↗
PubMed1988

Importance of carbonic anhydrase for canalicular and ductular choleresis in the pig.

To assess the importance of carbonic anhydrase (CA) for canalicular and ductular choleresis, the effect of acetazolamide on bile secretion was measured in three experimental groups of anaesthetized pigs. CA activity in liver homogenate was 46 (43-54) U g-1 wet weight, 150 mg kg-1 b.w. acetazolamide completely abolished the CA activity. Acetazolamide reduced bile HCO3- secretion in six secretin infused, bile-acid depleted pigs by 67 (58-71)% at arterial pH 7.41 (7.38-7.46). By contrast, acetazolamide did not affect HCO3- secretion in six Na-taurocholate (TCA) infused pigs in the absence of secretin stimulation. Acetazolamide reduced ursodeoxycholic-acid- (UDCA) dependent HCO3- secretion by 24 (11-38)% in six other pigs in the absence of secretin stimulation. Histochemical examination using modifications of Hansson's method showed strong reaction in bile ductules and weaker reaction in peripheral zones of liver lobules. Because acetazolamide impairs HCO3- secretion from cells sustaining high rates of H+/HCO3- transport, it is suggested that high rates of H+/HCO3- transport are confined to bile ductules under conditions of secretin- and UDCA-induced choleresis.

Acetazolamide↗
PubMed1992

Prevention of acute postoperative pressure rises in glaucoma patients undergoing cataract extraction with posterior chamber lens implant.

Acute elevations in intraocular pressure (IOP) commonly follow extracapsular cataract extraction and lens implant in glaucoma patients. Thirty six patients with glaucoma undergoing cataract extraction and posterior chamber lens implantation received one of three treatments. Group 1: 500 mg of Diamox Sustets (acetazolamide) 1 hour preoperatively (10 patients); Group 2: peroperative intracameral Miochol (acetylcholine) (11 patients); Group 3: the above treatments combined (15 patients). IOPs were measured at 3, 6, 9, and 24 hours postoperatively. The average of the maximum pressure rises above the preoperative level over the 24 hour period was greatest for the group receiving acetazolamide only at 8.9 mm Hg; for the acetylcholine group the average maximum rise was 6.3 mm Hg; while the combined treatment group showed a decrease of 0.7 mm Hg. IOP rises of > 6 mm Hg were seen in 7% of patients (one of 15) in the combined treatment group, 45% (five of 11) of the acetylcholine group, and 70% (seven of 10) of the acetazolamide group. IOP rises of > 10 mm Hg were seen in 7% of the combined treatment group, in 18% of the acetylcholine only group, and in 50% of the acetazolamide only group. A pressure rise > 20 mm Hg was seen in one patient receiving acetazolamide only and one patient receiving acetylcholine only. The difference between the acetylcholine group and the combined group for rises > 6 mm Hg was significant using the chi 2 test while the acetazolamide group showed a significant difference for rises > 6 and 10 mm Hg compared with the combined group. All acute pressure rises were recorded before or at 9 hours following operation except in the combined treatment patient where the rise occurred at 24 hours. To prevent the acute IOP rises seen following cataract surgery with lens implant in glaucoma patients we recommend combined ocular hypotensive therapy.

Acetazolamide↗
PubMed1986

Functional role of carbonic anhydrase in intestinal electrolyte transport.

We examined the role of carbonic anhydrase activity in intestinal transport by measuring the effect of systemic pH and PCO2 on electrolyte transport in the presence and absence of luminal acetazolamide. Adult Sprague-Dawley rats were anesthetized, and ileal and colonic segments were perfused with Ringer solution that was acetazolamide-free or that contained 0.1 mM sodium acetazolamide. Consecutive states of acute respiratory alkalosis and acidosis were created by changing the inspired CO2 from 0% (room air) to 8% CO2. In the ileum, acetazolamide perfusion did not affect the increment in net sodium and chloride absorption caused by a reduction in systemic pH. Mucosal carbonic anhydrase activity in this segment was measurable, although very low. In both the ascending and descending colon, acetazolamide perfusion reduced the increment in net sodium absorption caused by an increase in systemic PCO2. In addition, acetazolamide increased the chloride absorptive response to PCO2 in the ascending colon but did not affect the chloride response at all in the descending colon. Colonic mucosal carbonic anhydrase exhibited a proximal-to-distal gradient of activity: levels in the ascending colon were severalfold greater than in the descending colon. These findings suggest a functional role for carbonic anhydrase in mediating the colonic but not the ileal absorptive response to changes in systemic acid-base balance.

Acetazolamide↗
PubMed1998

Cyclooxygenase-2 participates in tubular flow-dependent afferent arteriolar tone: interaction with neuronal NOS.

To delineate the microvascular role of cyclooxygenase-2 (Cox-2) in modulating tubuloglomerular feedback (TGF) signals and to determine its relationship to neuronal nitric oxide synthase (nNOS), afferent (AA) and efferent (EA) arteriolar diameters of rat kidneys were assessed using the blood-perfused juxtamedullary nephron technique. The Cox-2 inhibitor NS-398 (10 microM) did not alter AA diameters in untreated kidneys but significantly constricted AAs by 17.0 +/- 2.2% in kidneys treated with 10 mM acetazolamide, which enhances TGF-mediated AA constriction by increasing distal volume delivery. The NS-398-induced AA constriction was prevented after interruption of distal delivery by transection of the loops of Henle. The effect was selective for AAs since NS-398 did not influence EAs of untreated or acetazolamide-treated kidneys. Pretreatment with the nNOS inhibitor S-methyl-L-thiocitrulline (10 microM) prevented the NS-398-induced AA constriction observed during acetazolamide treatment. Although we previously demonstrated that acetazolamide treatment enhanced AA constrictor response to S-methyl-L-thiocitrulline, the enhancement by acetazolamide was inhibited by pretreatment with 10 microM NS-398 (16.4 +/- 1.9 and 15. 0 +/- 0.5% with and without acetazolamide, respectively, P > 0.05). These results indicate that, during increased activation of TGF-dependent vasoconstrictor signals, Cox-2 generates vasodilatory metabolites in response to increased nNOS activity and thus participates in the counteracting modulation of TGF-mediated AA constriction.

Acetazolamide↗