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PubMed1998

Chloride and non-selective cation channels in unstimulated trout red blood cells.

1. The cell-attached and excised inside-out configurations of the patch-clamp technique were used to demonstrate the presence of two different types of ion channels in the membrane of trout red blood cells under isotonic and normoxic conditions, in the absence of hormonal stimulation. The large majority (93%) of successful membrane seals allowed observation of at least one channel type. 2. In the cell-attached mode with Ringer solution in the bath and Ringer solution, 145 mM KCl or 145 NaCl in the pipette, a channel of intermediate conductance (15-25 pS at clamped voltage, Vp = 0 mV) was present in 85% of cells. The single channel activity reversed between 5 and 7 mV positive to the spontaneous membrane potential. A small conductance channel of 5-6 pS and +5 mV reversal potential was also present in 62% of cells. 3. After excision into the inside-out configuration (with 145 mM KCl or NaCl, pCa 8 in the bath, 145 mM KCl or NaCl, pCa 3 in the pipette) the intermediate conductance channel was present in 439 out of 452 successful seals. This channel was spontaneously active in 90% of patches and in the other 10% of patches the channel was activated by suction. The current-voltage relationship showed slight inward rectification. The channel conductance was in the range 15-20 pS between -60 and 0 mV and increased to 25-30 pS between 0 and 60 mV, with a reversal potential close to zero. Substitution of K+ for Na+ in the pipette or in the bath did not significantly change the single channel conductance. Dilution of the bathing solution KCl concentration shifted the reversal potential towards the Nernst equilibrium for cations. Substitution of N-methyl-D-glucamine (NMDG) for K+ or Na+ in the bath almost abolished the outward current whilst the divalent cation Ca2+ permeated the channel with a higher permeability than K+ and Na+. Inhibition of channel openings was obtained with flufenamic acid, quinine, gadolinium or barium. Taken together these data demonstrate that the intermediate conductance channel belongs to a class of non-selective cation (NSC) channels. 4. In excised patches, under the same control conditions, the conductance of the small conductance non-rectifying channel was 8.6 +/- 0.8 pS (n = 12) between -60 and +60 mV and the reversal potential was close to 0 mV. This channel could be blocked by 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) but not by flufenamic acid, DIDS, barium or gadolinium. Selectivity and substitution experiments made it possible to identify this channel as a non-rectifying small conductance chloride (SCC) channel.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

Influence of limonene and laurocapram on percutaneous absorption of nonsteroidal anti-inflammatory drugs.

The promoting effect of cyclic monoterpenes, 1% limonene (CAS 5989-27-5) and 1% cineole (CAS 470-82-6), on percutaneous absorption of nonsteroidal anti-inflammatory drugs was investigated in the rats. Compared with 1% laurocapram, drug absorption from the gel ointments was significantly more enhanced by addition of 1% limonene, while without any enhancer only ibuprofen penetrated across the skin in the limited amount. When using formulation with propylene glycol or 50% propylene glycolethanol solution, instead of carboxyvinyl polymer gel, percutaneous absorption significantly decreased and neither limonene nor cineole or laurocapram were capale to promote percutaneous absorption of flufenamic acid to sufficient serum level. Cineole and limonene were also evaluated in permeation experiments in vitro. Enhancement ability of limonene in the gel oinment was approximately 5 times higher comparing with enhancement ratio of cineole, while in 100% propylene glycol enhancement ability of both cyclic monoterpenes was equal. Good correlation was observed between in vivo and in vitro experiments. Evaluation of solubility proved that in the gel ointment simulated as water-ethanol solution were relatively best condition for percutaneous absorption of flufenamic acid when comparing with propylene glycol or 50% propylene glycol-ethanol solution.

Administration, Topical↗
PubMed1982

Control of IUD-induced bleeding by three non-steroidal anti-inflammatory drugs.

Administration of nonsteroidal anti-inflammatory drugs (NSAIDs) reduced excessive IUD-induced bleeding. The effect of 3 different oral NSAIDs, namely indomethacin, Alclofenac, and flufenamic acid, on menstrual blood loss (MBL) and pain among women fitted with copper IUDs was studied and compared with a placebo on a randomized single blind basis. Each drug was given to 6 subjects (18 cases) over 2 consescutive cycles and was either preceded or followed by placebo for 2 more cycles. 1/2 of the cases on each drug started placebo medication in the 1st 2 months while the other 1/2 started by the drug. The oral treatment was begun on the 1st day of menstrual bleeding or spotting. Estimation of the daily MBL was done by the alkaline hematin method with mechanical extraction of sanitary pads. The 3 drugs tested in this study induced a significant reduction in MBL: maximum reduction by flufenamic acid medication, less with Alclofenac, and least with indomethacin medication. However, these reductions were not statistically different, and marked improvement in IUD-induced pain was observed under the effect of the 3 drugs.

Age Factors↗
PubMed1981

Dysmenorrhoea and prostaglandins: pharmacological and therapeutic considerations.

Primary dysmenorrhoea is characterised by painful menstrual cramps which appear to have no macroscopically identifiable pelvic pathology. 50% of postpubescent females suffer from dysmenorrhoea, and 10% are incapacitated for 1 to 3 days each month. Many of these patients have an increased synthesis of prostaglandins in their endometrial tissue with increased prostaglandin release in the menstrual fluid. The increased amount of prostaglandins induces incoordinate hyperactivity of the uterine muscle resulting in uterine ischaemia and pain. Recent clinical and laboratory studies have shown that many of the non-steroidal anti-inflammatory drugs such as ibuprofen, naproxen, flufenamic acid, mefenamic acid and indomethacin are capable of relieving primary dysmenorrhoea. These drugs are inhibitors of the prostaglandin synthetase enzymes which are necessary for prostaglandin biosynthesis. Thus, with ibuprofen it has been shown that clinical relief of the dysmenorrhoeic symptoms accompanies the reduction of menstrual fluid prostaglandins. With the oral contraceptive pill there is good relief of primary dysmenorrhoea, significant decrease in menstrual fluid prostaglandins, but no reduction in menstrual fluid volume; this suggests that the reduction in prostaglandins is secondary to the inhibition of endometrial growth and development. In some forms of secondary dysmenorrhoea elevated prostaglandin levels have been implicated. However, the evidence is less conclusive for dysmenorrhoea secondary to endometriosis and uterine myomas than for dysmenorrhoea associated with intrauterine devices. With the intrauterine device, prostaglandin synthetase inhibitors such as flufenamic acid, ibuprofen and naproxen are able not only to relieve dysmenorrhoea but also to reduce menstrual blood loss to normal levels. Thus, the use of appropriately selected prostaglandin synthetase inhibitors can offer effective relief from the miseries of some types of dysmenorrhoea with subsequent restoration of normal daily activities.

Adolescent↗
PubMed1986

Effects of DNA and prostaglandin synthesis inhibitors on the stimulation of bone resorption by epidermal growth factor in fetal rat long-bone cultures.

We examined two inhibitors of DNA synthesis, hydroxyurea (HU) and aphidicholin (APC), and two inhibitors of prostaglandin cyclooxygenase, indomethacin and flufenamic acid, for their effects on the resorptive responses of fetal rat long-bone cultures to epidermal growth factor (EGF) and parathyroid hormone (PTH). As we have previously found, HU decreased unstimulated 45Ca release but had little effect on the resorptive response to PTH. HU also did not block resorption stimulated by EGF. Addition of the cyclooxygenase inhibitor, indomethacin, did not alter the resorptive responses of unstimulated or PTH-treated cultures in either the presence or absence of HU or the resorptive response of bones cultured with EGF alone. However, indomethacin completely blocked the resorptive response to EGF of bones that were cultured with HU. The effects of indomethacin on EGF-mediated resorption in HU-treated cultures appeared to be related to an inhibition of prostaglandin synthesis since flufenamic acid had similar effects. However, the effects of HU on the resorptive response to EGF may not have resulted solely from its inhibitory action on DNA synthesis since APC, in the absence of cyclooxygenase inhibitors, completely blocked EGF-mediated resorption without significantly affecting the response to PTH. These results demonstrate that the mechanisms regulating PTH- and EGF-mediated resorption in fetal rat long-bone cultures differ, and imply that a component of EGF-mediated resorption in these cultures is dependent on sustained DNA synthesis.

Animals↗
PubMed1999

Sequential activation of different Ca2+ entry pathways upon cholinergic stimulation in mouse pancreatic acinar cells.

1. We have studied capacitative calcium entry (CCE) under different experimental conditions in fura-2-loaded mouse pancreatic acinar cells by digital microscopic fluorimetry. CCE was investigated during [Ca2+]i decay after cell stimulation with a supramaximal concentration of ACh (10 microM) or during Ca2+ readmission in Ca2+-depleted cells (pretreated with thapsigargin or ACh). 2. La3+ and Zn2+ (100 microM) inhibited CCE during Ca2+ readmission but had negligible effects during ACh decay. In contrast flufenamic acid (100 microM), an inhibitor of non-selective cation channels, genistein (10 microM), a broad-range tyrosine kinase inhibitor, and piceatannol (10 microM), an inhibitor specific for non-receptor Syk tyrosine kinase, inhibited CCE during ACh decay but not during Ca2+ reintroduction. 3. Simultaneous detection of Mn2+ entry and [Ca2+]i measurement showed that, in the presence of extracellular calcium, application of 100 microM Mn2+ during ACh decay resulted in manganese influx without alteration of calcium influx, whilst when applied during Ca2+ readmission, Mn2+ entry was significantly smaller and induced a clear inhibition of CCE. 4. Application of the specific protein kinase C inhibitor GF109293X (3 microM) reduced CCE in Ca2+-depleted cells, whereas the activator phorbol 12-myristate, 13-acetate (3 microM) increased Ca2+ entry. 5. Based on these results we propose that cholinergic stimulation of mouse pancreatic acinar cells induces Ca2+ influx with an initial phase operated by a non-specific cation channel, sensitive to flufenamic acid and tyrosine kinase inhibitors but insensitive to lanthanum and divalent cations, followed by a moderately Ca2+-selective conductance inhibited by lanthanum and divalent cations.

Acetylcholine↗
PubMed1979

[Some experiments on the allergic reaction among workers in a pharmaceutical factory (author's transl)].

A survey was made on workers handling powdered drugs in a pharmaceutical factory. In this factory, two kinds of anti-inflammatory enzyme (bromelain and trypsin), one anti-inflammatory agent (flufenamic acid), one antispasmodic (flopropion) and two kinds of antibiotics (ampicillin and cephalexin) are mainly produced. Twenty four workers were examined by interviews and checked by Cornell Medical Index, and 18 of them complained of respiratory symptoms. These 18 workers were physically examined by skin scratch tests, pulmonary function tests and serum immunological tests. Among 24 workers, 9 handled powdered drugs (A group), 5 handled the same in the past and had already been transferred to other sections for their symptoms (B group), 3 engaged in the process of capsul-filling (C group) and 7 handled several times occasionally during one year (D group). Their average months spent in handling powdered drugs were, in the case of anti-inflammatory enzyme, A group 53.2, B group 66.2, and in the case of antibiotics, 5 workers in A group 24.0, 2 workers in B group 7.0, 3 workers in C group 25.7. Twenty workers complained of symptoms which were mainly irritation of mucosa including the respiratory system and itching of the skin while they were working, and accelerated nasal discharge, urticaria and asthma after working. Group A and group B were higher than group D in the rate of respiratory complaints in C.M.I. (p less than 0.001). Fourteen workers pointed out anti-inflammatory enzyme as a cause of main symptoms, 7 workers flufenamic acid, 3 workers flopropion, 4 workers antibiotics. Three workers who had past history of asthma or articular rheumatism had been transferred to other sections. Of 18 workers who were physically examined, 11 workers showed positive reactions to skin scratch tests with handling drugs. On 8 workers of them, some kinds of drugs which were pointed out as drugs causing main symptoms reacted positively. Numbers of workers with increased immunoglobin values were, IgE 3, IgM 2, IgA 4, IgM 2. Two workers showed decreased FVC and FEV (1.0 sec.) values in pulmonary function tests. The causes of the occupational allergic reaction in this factory are guessed as follows: 1) control of powdered materials was incomplete in the process of production, 2) various kinds of sensitizing drugs were handled by the same workers.

Adult↗
PubMed1995

Influence of extracellular Ca2+ on endogenous Cl- channels in Xenopus oocytes.

Removal of Ca2+ from the external bath solution evoked marked depolarization and large currents (up to several microamperes) in voltage-clamped defolliculated oocytes of Xenopus laevis. The resulting current was not carried by a cation influx but was due to a huge Cl- efflux, which could be strongly inhibited by the Cl- channel blockers flufenamic acid and niflumic acid. Removal of Mg2+ or Ba2+ from the solutions had the same effects as removing Ca2+. The reversal potential of -12 mV also indicated that Cl- channels were responsible for the large currents. Patch-clamp studies revealed a single-channel slope conductance of 90 pS. During oocyte maturation these channels remained active. The half-maximal Ca2+ concentration of about 20 microM showed that quite low doses of extracellular Ca2+ profoundly influence the electrical properties of the oocyte membrane.

Animals↗
PubMed1976

Reduction of menstrual blood-loss by prostaglandin-synthetase inhibitors.

Six patients with menorrhagia due to dysfunctional uterine bleeding and one patient with an intrauterine contraceptive device were treated with prostaglandin-synthetase inhibitors in an attempt to reduce their excessive menstrual blood-loss. Mefenamic acid (six patients) or flufenamic acid (one patient) taken during menstruation for 2-3 cycles reduced menstrual loss in each patient. These preliminary observations suggest a new treatment for a common gynaecological problem and could imply that prostaglandins are involved in the aetiology of excessive menstrual blood-loss in such patients.

Adult↗
PubMed1994

Drug competition for intracellular triiodothyronine-binding sites.

A variety of substances, including frusemide, non-esterified fatty acids (NEFAs) and non-steroidal anti-inflammatory drugs (NSAIDs), can compete for triiodothyronine (T3)-binding sites in serum and at the cell surface. We examined the competitive potency of these agents at intracellular T3-binding sites in order to assess their potential to act as T3 antagonists. Competition for [125I]T3 binding was determined using hydroxyapatite separation in cytosols and nuclear extracts prepared from livers of Macaca fascicularis. The T3 affinities were 15.8 +/- 1.2 nmol/l in cytosol and 0.23 +/- 0.02 nmol/l in nuclear extract. Dose-response curves were analysed by a four-parameter sigmoid curve-fitting program to determine competitor potency. The nineteen agents tested included various NSAIDs, NEFAs, non-bile acid cholephils (NBACs), frusemide, amiodarone and the flavonoid EMD 21388. In nuclear extract the most active competitors were linoleic acid (8.5 mumol/l) and linolenic acid (7.8 mumol/l). Potencies of NSAIDs varied between 66 mumol/l (meclofenamic acid) and 525 mumol/l (diclofenac). In cytosol, NEFAs were less potent but NSAIDs were stronger competitors than in nuclear extract. Half-inhibitory potencies in cytosol were between 13.2 mumol/l (meclofenamic acid) and 63.1 mumol/l (flufenamic acid). The NBAC bromosulphthalein was one of the most potent inhibitors in both cytosol and nuclear extract. When expressed relative to T3, diclofenac was a more effective competitor in cytosol than it was in nuclear extract. Amiodarone and EMD 21388 were without effect both in cytosol and nuclear extract. Frusemide (759 mumol/l) was weakly active in cytosol only.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗
PubMed1998

Inhibiting transthyretin conformational changes that lead to amyloid fibril formation.

Insoluble protein fibrils resulting from the self-assembly of a conformational intermediate are implicated as the causative agent in several severe human amyloid diseases, including Alzheimer's disease, familial amyloid polyneuropathy, and senile systemic amyloidosis. The latter two diseases are associated with transthyretin (TTR) amyloid fibrils, which appear to form in the acidic partial denaturing environment of the lysosome. Here we demonstrate that flufenamic acid (Flu) inhibits the conformational changes of TTR associated with amyloid fibril formation. The crystal structure of TTR complexed with Flu demonstrates that Flu mediates intersubunit hydrophobic interactions and intersubunit hydrogen bonds that stabilize the normal tetrameric fold of TTR. A small-molecule inhibitor that stabilizes the normal conformation of a protein is desirable as a possible approach to treat amyloid diseases. Molecules such as Flu also provide the means to rigorously test the amyloid hypothesis, i.e., the apparent causative role of amyloid fibrils in amyloid disease.

Amino Acid Sequence↗
PubMed1993

Novel instrumentation and biomedical applications of very near infrared fluorescence.

A high wavelength fluorescent probe, Nile Red, was added to four proteins, viz., bovine albumin, alpha 1-acid glycoprotein, beta-lactoglobulin and ovomucoid. Nile Red showed an enhancement in fluorescence and a shift in emission wavelength, suggesting it was bonding hydrophobically to these proteins. Drug displacement of Nile Red from alpha 1-acid glycoprotein was achieved with both D,L-propranolol and flufenamic acid, showing that the binding site is less electrostatic and more hydrophobic in nature. In order to monitor these interactions, a simple spectrofluorimeter was constructed from solid-state components; the sensitivity of this instrument compared well with that of standard laboratory spectrofluorimeters.

Binding Sites↗
PubMed1983

Suppression of tumor promoter phorbolmyristate acetate-induced chromosome breakage by antioxidants and inhibitors of arachidonic acid metabolism.

To gain insight into the mechanism of formation of chromosomal aberrations by the tumor promoter phorbolmyristate acetate (PMA) in human lymphocytes, we investigated the effect of antioxidants and inhibitors of arachidonic acid metabolism. Among the antioxidants bovine erythrocyte CuZn superoxide dismutase, glutathione peroxidase, mannitol (a scavenger of hydroxyl radicals), butylated hydroxytoluene and butylated hydroxyanisole were anticlastogenic while catalase and dimethylfuran (a scavenger of singlet oxygen) were inactive. These results show that the induction of aberrations by PMA occurs via indirect action, i.e. the intermediacy of superoxide and hydroxyl radicals. The following inhibitors of arachidonic acid metabolism were strongly anticlastogenic: the cyclo-oxygenase inhibitors indomethacin and flufenamic acid and the lipoxygenase inhibitor BN1015. Imidazole, nordihydroguaiaretic acid BN1048 and 5,8,11,14-eicosatetraynoic acid were moderately active. The inhibitor of phospholipase A2, fluocinolone acetonide, was also anticlastogenic. We conclude that the oxidative metabolism of arachidonic acid is involved in the induction of chromosomal aberrations by PMA in human lymphocytes. However, because of the limited selectivity of these drugs, it is not yet possible to identify unambiguously the step(s) in the arachidonic acid cascade responsible for PMA clastogenicity.

Anti-Inflammatory Agents↗
PubMed2004

Activation of a calcium-activated cation current during epileptiform discharges and its possible role in sustaining seizure-like events in neocortical slices.

Epileptic seizures are composed of recurrent bursts of intense firing separated by periods of electrical quiescence. The mechanisms responsible for sustaining seizures and generating recurrent bursts are yet unclear. Using whole cell voltage recordings combined with intracellular calcium fluorescence imaging from bicuculline (BCC)-treated neocortical brain slices, I showed isolated paroxysmal depolarization shift (PDS) discharges were followed by a sustained afterdepolarization waveform (SADW) with an average peak amplitude of 3.3 +/- 0.9 mV and average half-width of 6.2 +/- 0.6 s. The SADW was mediated by the calcium-activated nonspecific cation current (I(can)) as it had a reversal potential of -33.1 +/- 6.8 mV, was unaffected by changing the intracellular chloride concentrations, was markedly diminished by buffering [Ca(2+)](i) with intracellular bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA), and was reversibly abolished by the I(can) blocker flufenamic acid (FFA). The Ca(2+) influx responsible for activation of I(can) was mediated by both N-methyl-d-aspartate-receptor channels, voltage-gated calcium channels and, to a lesser extent, internal calcium stores. In addition to isolated PDS discharges, BCC-treated brain slices also produced seizure-like events, which were accompanied by a prolonged depolarizing waveform underlying individual ictal bursts. The similarities between the initial part of this waveform and the SADW and the fact it was markedly reduced by buffering [Ca(2+)](i) with BAPTA strongly suggested it was mediated, at least in part, by I(can). Addition of FFA reversibly eliminated recurrent bursting, and transformed seizure-like events into isolated PDS responses. These results indicated I(can) was activated during epileptiform discharges and probably participated in sustaining seizure-like events.

Animals↗
PubMed1995

Flow-injection spectrofluorimetric determination of flufenamic and mefenamic acid in pharmaceuticals.

Two sensitive and rapid flow-injection (FI) spectrofluorimetric methods are proposed for the determination of flufenamic acid (FF) and mefenamic acid (MF), based on the formation of complexes of these compounds with A1(III) in an ethanolic medium. The calibration graphs resulting from the measurements of the fluorescence at lambda exc = 351 nm and lambda em = 440 nm, and lambdaexc = 355 nm and lambda em = 454 nm for the complexes with FF and MF, respectively, are linear over the range 0.030-1.20 micrograms ml-1 for FF and 0.30-16.1 micrograms ml-1 for MF. The methods have been applied to the determination of these drugs in pharmaceutical preparations.

Administration, Topical↗
PubMedDate not supplied

Etofenamate fatty acid asters. An example of a new route of drug metabolism.

Etofenamate [2-(2-hydroxyethoxy)ethyl-N-(alpha, alpha, alpha-trifluoro-m-tolyl)-anthranilate] was administered to dogs by the oral route. Minor amounts of etofenamate (Eto) and its glucuronide were found in urine and feces. The main portion of metabolites was eliminated as flufenamic acid (Flu) and hydroxy derivatives of Eto and Flu. Furthermore, a highly lipophilic fraction was isolated (extraction and TLC) and further separated into several compounds (HPLC, GLC). These metabolites were identified as Eto oleate, palmitate, linoleate, stearate, palmitoleate, myristate, and laurate by NMR and MS. The structures were confirmed by comparison with authentic material. The conjugation of etofenamate with fatty acids is an example of a new route of drug metabolism.

Administration, Oral↗
PubMed1997

Unexpected and differential effects of Cl- channel blockers on the Kv4.3 and Kv4.2 K+ channels. Implications for the study of the I(to2) current.

The Kv4.3 K+ channel is thought to underlie the Ca(2+)-insensitive transient outward current (I(to1)) in ventricular myocytes of canine and human heart and to contribute to the I(to1) in rat myocytes. It has been suggested that there is a second component of the transient outward current in some species that is contributed by a Ca(2+)-activated Cl- current (known as I(to2)). The evidence for the existence of the I(to2) current is based, in part, on the pharmacological effects of various Cl- channel blockers. To test for possible interactions between these compounds and I(to1), the effect of several different Cl- channel blockers on the Kv4.3 channel was examined. The fenamates (niflumic and flufenamic acid) were found to have large effects on the position of the steady state inactivation curve of the Kv4.3 channel. The disulfonic stilbenes (DIDS and SITS) had markedly different effects and were found to greatly reduce the rate of recovery from inactivation of the Kv4.3 channel without large changes in the position of the activation and steady state inactivation curves. Both classes of drugs produced an apparent blockade of the Kv4.3 channel under some recording conditions. Surprisingly, the closely related Kv4.2 channel was found to be markedly less sensitive to these drugs. Caffeine was found to block both the Kv4.3 and Kv4.2 channels to a similar extent. These nonspecific drug effects have implications for the study of the two components of the transient outward current and suggest that purely pharmacological criteria cannot be used to define the physiological role of I(to2).

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1984

Effect of hyperosmotic xylitol on gastric secretion in the rat: lack of influence of cyclooxygenase inhibitors.

The effects of hyperosmotic solutions of xylitol were tested on acid and bicarbonate outputs from the rat stomach as well as on acid back-diffusion. Hyperosmotic solutions were instilled into anesthetized rats by an esophageal cannula and drained through a duodenal catheter. Spontaneously secreting and histamine-stimulated rats were used in different experiments. Hyperosmotic xylitol solutions at concentrations of 18.4% or higher produced graded inhibitions of the histamine-induced acid secretion. A 34.5% xylitol solution also inhibited spontaneous acid secretion. The same solution also caused a certain degree of acid back-diffusion and increased output of bicarbonate. Neither the inhibition acid secretion nor stimulation of bicarbonate output were affected by cyclooxygenase inhibitors indomethacin or flufenamic acid. It is concluded that hyperosmotic xylitol reduces gastric acidity by three mechanisms namely inhibition of acid secretion, increased bicarbonate output and increased back-diffusion of acid. None of these mechanisms seem to depend on prostaglandin biosynthesis.

Animals↗