Biomedical subjects

E Ferrary

Publications and source records attributed to E Ferrary.

At least 37 records · Page 2Linked to original sources

PubMed1999

Parathyroid hormone-parathyroid hormone-related peptide receptor expression and function in otosclerosis.

The aim of this study was to investigate the possibility that an abnormality related to parathyroid hormone (PTH) action is involved in the increased bone turnover observed in otosclerosis. To do so, expression and function of the PTH-PTH-related peptide (PTHrP) receptor were studied in the involved tissue (stapes) and compared with that in control bone sample obtained from the external auditory canal (EAC) in the same patient in 10 cases of otosclerosis and in 1 case of osteogenesis imperfecta. PTH-PTHrP receptor expression was studied by RT-PCR of RNA prepared from cultured cells in three patients and RNA directly extracted from bone samples in four patients. PTH-PTHrP receptor function was assessed by measuring the stimulation of cAMP production by 0.8, 8, and 80 nM PTH in bone cell cultures in seven cases. Results showed that PTH-PTHrP receptor mRNA expression in the otosclerotic stapes was lower than that in EAC samples (P < 0.05), whereas it was higher in stapes than that in EAC in the case of osteogenesis imperfecta. cAMP production after PTH stimulation was lower in bone cells cultured from otosclerotic stapes compared with that in cells cultured from EAC (range of increase in stimulation: 0.8-4.5 and 1.5-7 in stapes and EAC bone cells, respectively, P < 0.05). In contrast, the stimulation of cAMP production by forskolin was not significantly different in otosclerotic stapes and EAC bone cells (range of increase in stimulation: 20.7-83.1 and 4.9-99.8 in stapes and EAC, respectively, P > 0.05). These results show a lower stimulation of cAMP production in response to PTH associated with a lower PTH-PTHrP receptor mRNA expression in pathological stapes from patients with otosclerosis compared with that in control EAC samples. This difference supports the hypothesis that an abnormal cellular response to PTH contributes to the abnormal bone turnover in otosclerosis.

Adult↗

PubMed1998

Taurine entry into perilymph of the guinea pig.

Taurine is a beta-aminosulfonic acid and is a ubiquitous amino acid whose role in the cochlea is not well established. In this study, its entry from blood into perilymph was investigated in the guinea pig as animal model. The penetration rate of [3H]taurine (molecular weight 125) into the perilymph of the scala vestibuli was measured 1 and 2 h after the intravenous infusion of [3H]taurine in nephrectomized animals. Results showed a rate of penetration in perilymph related to plasma at 36 +/- 4.7% (n = 5) after 1 h and 43 +/- 5.6% (n = 5) after 2 h. Compared to the penetration rate of urea (molecular weight 60) and mannitol (molecular weight 186) reported previously in rats, a passive entry of taurine into perilymph through the blood-perilymph barrier is suggested.

Animals↗

PubMed1998

The effects of perilymphatic tonicity on endolymph composition and synaptic activity at the frog semicircular canal.

The effects of changes in perilymphatic tonicity on the semicircular canal were investigated by combining the measurements of transepithelial potential and endolymphatic ionic composition in the isolated frog posterior canal with the electrophysiological assessment of synaptic activity and sensory spike firing at the posterior canal in the isolated intact labyrinth. In the isolated posterior canal, the endolymph was replaced by an endolymph-like solution of known composition, in the presence of basolateral perilymph-like solutions of normal (230 mosmol/kg), reduced (105 mosmol/kg, low NaCl) or increased osmolality (550 mosmol/kg, Na-Gluconate added). Altered perilymphatic tonicity did not produce significant changes in endolymphatic ionic concentrations during up to 5 min. In the presence of hypotonic perilymph, decreased osmolality, K and Cl concentrations were observed at 10 min. In the presence of hypertonic perilymph, the endolymphatic osmolality began to increase at 5 min and by 10 min Na concentration had also significantly increased. On decreasing the tonicity of the external solution an immediate decline was observed in transepithelial potential, whereas hypertonicity produced the opposite effect. In the intact frog labyrinth, mEPSPs and spike potentials were recorded from single fibers of the posterior nerve in normal Ringer's (240 mosmol/kg) as well as in solutions with modified tonicity. Hypotonic solutions consistently decreased and hypertonic solutions consistently increased mEPSP and spike frequencies, independent of the species whose concentration was altered. These effects ensued within 1-2 min after the start of perfusion with the test solutions. In particular, when the tonicity was changed by varying Na concentration the mean mEPSP rate was directly related to osmolality. Size histograms of synaptic potentials were well described by single log-normal distribution functions under all experimental conditions. Hypotonic solutions (105 mosmol/kg) markedly shifted the histograms to the left. Hypertonic solutions (380-550 mosmol/kg, NaCl or Na-Gluconate added) shifted the histograms to the right. Hypertonic solutions obtained by adding sucrose to normal Ringer's solution (final osmolality 550 mosmol/kg) increased mEPSP and spike rates, but did not display appreciable effects on mEPSP size. All effects on spike discharge and on mEPSP rate and size were rapidly reversible. In Ca-free, 10 mM EGTA, Ringer's solution, the sensory discharge was completely abolished and did not recover on making the solution hypertonic. These results indicate that perilymphatic solutions with altered tonicity produce small and slowly ensuing changes in the transepithelial parameters which may indirectly affect the sensory discharge rate, whereas relevant, early and reversible effects occur at the cytoneural junction. In particular, the modulation of mEPSP amplitude appears to be postsynaptic; the presynaptic effect on mEPSP rate of occurrence is presumably linked to local calcium levels, in agreement with previous results indicating that calcium inflow is required to sustain basal transmitter release in this preparation.

Action Potentials↗

PubMed1998

Effect of locally applied drugs on the endolymphatic sac potential.

In Ménière's disease, an inner ear disorder related to an endolymphatic hydrops, an alteration of the functioning of the endolymphatic sac has been proposed. The endolymphatic sac is assumed to be involved in the secretion/resorption of endolymph. The epithelial transport systems have been indirectly studied by the recording of the endolymphatic sac transepithelial potential (ESP) in control conditions and after the local injection of drugs such as diuretics that have been proposed in the treatment of Ménière's disease. The ESP was recorded, in vivo, in guinea pigs up to 150 minutes after the perisaccular injection of 5 microL of a 150 mmol/L (mM) NaCl solution containing various drugs known to inhibit ionic transport systems. The initial ESP was +8.4+/-0.3 mV (mean +/- SEM, n = 78). The basolateral injection of 5 microL of 150 mM NaCl induced an ESP decrease of 64%+/-6.0% (n = 12), 5 minutes after the end of the injection. Then ESP increased, returning to its initial value at 60 minutes and surpassing it at 120 minutes. Diuretics such as acetazolamide (10[-3] mol/L [M]), an inhibitor of carbonic anhydrase, and amiloride (10[-4] M), an inhibitor of Na channel or Na/H exchanger, decreased the ESP recovery. At variance, bumetanide (10[-6] M, 10[-4] M), the Na-K-Cl cotransport inhibitor, and chlorothiazide (10[-4] M), a Na-Cl cotransporter inhibitor, failed to alter the ESP as compared with the control group. Ouabain (10[-3] M), the Na+,K+-adenosine triphosphatase (ATPase) inhibitor, prevented the ESP recovery otherwise observed 60 minutes after the NaCl injection. Bafilomycin A1, the inhibitor of the vacuolar-type H+-ATPase, prevented the recovery of the ESP with a log-dose/effect (10[-5] M, 10[-6] M, 10[-8] M). Disulfonic acid stilbene (DIDS) (10[-4] M), an inhibitor of transporters involving HCO3-, also prevented the ESP recovery. These results suggest that the genesis of the ESP was highly dependent on acid-base transport systems including carbonic anhydrase, a vacuolar-type H+-ATPase, and an anionic transport system blocked by DIDS. Further studies are needed to confirm the alteration of the acid-base balance in this epithelium and its possible involvement in the pathogenesis of Ménière's disease.

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

PubMed1998

Pharmacological characterization of ATP receptors in ampulla from frog semicircular canal.

Phosphoinositidase C activities sensitive to purine and pyrimidine nucleotides have been identified earlier in ampulla from Rana ridibunda semicircular canal. The aim of this study was to characterize the pharmacological properties of other P2 receptors borne by this structure. A microassay was developed to measure the binding of [35S]adenosine 5'-O-(2-thiodiphosphate) ([35S]ADPbetaS) to a few ampullas microdissected from frog semicircular canals. When determined at 4 degrees C in the absence of divalent cations, [35S]ADPbetaS binding was saturable with incubation time and reversible after elimination of free radioligand. The dissociation kinetics were biphasic and comprised a major component that was rapidly reversible and a minor component that dissociated slowly. [35S]ADPbetaS binding was competitively inhibited by unlabeled ADPbetaS with an apparent dissociation constant of 0.48 +/- 0.09 microM and a Hill coefficient of 0.70 +/- 0.06, and Scatchard analysis revealed a minor class of high-affinity binding sites (RT1 = 52 +/- 11 fmol [35S]ADPbetaS bound/ampulla and Kd1 = 0.15 +/- 0.04 microM) and a major class of low-affinity binding sites (RT2 = 436 +/- 79 fmol [35S]ADPbetaS bound/ampulla and Kd2 = 2.0 +/- 0.8 microM). The pattern of stereospecificity for recognition of unlabeled structural ATP analogs was ADPbetaS >/= alpha, beta-methyleneadenosine 5'-triphosphate = ADP = adenosine 5'-O-(3-thiotriphosphate) > ATP = diadenosine tetraphosphate = AMP > 2'- and 3'-O-(4-benzoylbenzoyl)-adenosine 5'-triphosphate >/= 2-methylthioadenosine 5'-triphosphate > 2-desoxythymidine 5'-triphosphate = guanosine 5'-triphosphate = inosine-5'-triphosphate = xanthosine 5'-triphosphate = cytosine 5'-triphosphate = uridine 5'-triphosphate = uridine-5'-diphosphate, whereas cAMP and adenosine were devoid of activity. For antagonists, suramin revealed competitive inhibitor potencies, whereas reactive blue 2 and DIDS acted as pure noncompetitive inhibitors. Results suggest that the population of labeled receptors is heterogeneous and contains a low number of P2Y-like receptors and a large number of P2X-like receptors whose molecular subtypes and functions in endolymph homeostasis remain to be defined.

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

PubMed1998

Mechanisms of endolymph secretion.

In the inner ear, the membranous labyrinth, a tight heterogeneous sensory epithelium, separates two compartments that are filled with fluids of completely different composition. The lumen of the membranous labyrinth is filled with endolymph, a K-rich, positively polarized fluid, whereas the surrounding spaces are filled with perilymph, with a composition similar to an usual extracellular fluid. The inner ear fluids play a major role in the cochlear and vestibular physiology by the transmission of the mechanical stimulus to the hair cells, on the one hand, and by the transduction of this signal to a nerve potential, on the other hand. Numerous studies have been performed in order to know the chemical and physical characteristics of the inner ear fluids. A high, positive transepithelial potential has been evidenced in the cochlea together with a high K concentration and a low Na concentration. During the last years, the composition of the inner ear fluids, the origins of endolymph and perilymph, and the cellular mechanisms involved in the secretion of these fluids have been a great part elucidated. The present paper is a review of the contribution of the lab to the understanding of the physiology of the inner ear.

Animals↗

PubMed1997

Paracellular transport properties of inner ear barriers do not account for cisplatin toxicity in the rat.

The interindividual variability for the ototoxic effect of the antineoplastic drug cisplatin has still to be explained. To examine if the variability can be related to differences in drug kinetics, the effect of cisplatin on the paracellular transport properties of the inner ear barriers was studied in vivo in cisplatin treated Long-Evans rats. The concentration of [3H]mannitol was followed in plasma, scala vestibuli perilymph, and endolymph after an intravenous infusion of the tracer. Cisplatin had no effect on paracellular transport of the inner ear barriers 3 days after administration of 8 mg/kg cisplatin. However, an interindividual variability for the transport of [3H]mannitol across the blood-perilymph barrier was evident, indicating a variability for the passive transport of solutes to the inner ear.

Animals↗

PubMed1997

Purine and pyrimidine nucleotide-sensitive phosphoinositidase C in ampulla from frog semicircular canal.

A microassay was developed to screen the abilities of ATP analogues to stimulate phosphoinositidase C in single ventral regions (including dark cells and sensory cells) of ampullas microdissected from posterior vertical semicircular canals of Rana ridibundo and labeled with myo-[3H]inositol. ATP induced a dose-dependent and saturable increase of total [3H]linositol phosphate production accompanied by an equivalent decrease in the [3H]phosphoinositide pool. The rank order of analogues revealing agonistic potencies for phosphoinositidase C activation was as follows: uridine 5'-triphosphate > or = adenosine 5'-O-[3-thiophosphate] tetralithium > adenosine 5'-O-[2-thiodiphosphate] trilithium > or = ATP > or = ADP = inosine 5'-triphosphate > or = guanosine 5'-triphosphate > or = 2-methylthio-adenosine 5'-triphosphate tetrasodium > or = 2'-desoxy-thymidine 5'-triphosphate > or = cytidine 5'-triphosphate = (alpha, beta)-methyl ATP > AMP, whereas adenosine 3',5'-cyclic monophosphate and adenosine were almost devoid of activity. For antagonists, 1,4'-diisothiocyanostilbene-2, 2'-disulfonic acid was far more active than suramin for competitive inhibition of ATP-induced enzyme stimulation, whereas reactive blue 2 acted as a noncompetitive inhibitor. Results indicate that the putative P2 receptors triggering phosphoinositidase C activation in ventral ampullary epithelium from frog semicircular canal exhibit mainly the functional properties of P2Y and P2U receptors.

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

PubMed1996

The effect of clofilium, a K-channel blocker, on the electrogenic K secretion and the sensory discharge at the frog semicircular canal.

Potassium transport by dark cells produces marked K-concentration differences between endo- and perilymphatic fluids in labyrinthine organs and generates the transepithelial potential. The ensuing electrochemical potential for K sustains the transduction current which regulates activity at the cytoneural junction. Clofilium, a compound which is known to block cardiac K channels and to decrease the endocochlear potential, was applied to the endolymphatic side of the isolated frog semicircular canal. The drug abolished the transepithelial potential and increased K outflux from the lumen to the dark cells (or the basolateral perilymph) with no apparent interference with active K secretion. When applied to the perilymphatic side in the intact labyrinth, clofilium reduced the rate of occurrence of miniature excitatory postsynaptic potentials (mEPSPs), both at rest and in response to mechanical stimulation (sinusoidal rotation at 0.1 Hz, 12.5 deg/s2 peak acceleration). This effect may be related to a reduced K-electrochemical unbalance and a decreased transduction current. The drug consistently reduced mEPSP size, although amplitude distributions remained log-normal and time intervals between successive mEPSPs remained exponentially distributed; this suggests a direct effect of clofilium on the postsynaptic membrane, in addition to any possible presynaptic effects. Spike discharge by the afferent fibre was almost completely abolished at rest and responses to mechanical stimulation were reduced by 85-90%. These effects cannot be accounted for by the mild reduction of mEPSP rates and confirm a direct action of clofilium on the afferent postsynaptic terminal.

Animals↗

PubMed1996

Hormonal modulation of inner ear fluids.

In the cochlea, hormones such as antidiuretic hormone and adrenocorticosteroid hormones are supposed to modulate the endolymph osmolality acting on the labyrinthine water permeability, on the one hand, and on the Na+, K(+)-ATPase, on the other hand. To test the hypothesis that these hormones are involved in the inner ear fluids homeostasis, the electrochemical composition of cochlear fluids was studied in control Long Evans rats, Brattleboro rats that are genetically deprived of antidiuretic hormone, and in adrenalectomized Long Evans rats. The results demonstrated that: i) in Brattleboro rats, the endocochlear K gradient was absent whereas the endocochlear potential and the Cl concentration gradients were maintained; the K gradient was restored by the dDAVP administration; ii) in adrenalectomized rats, no modification of the electrochemical composition of endolymph occurred; the injection of bumetanide (10 mg/kg) induced a larger decrease of the endocochlear potential in adrenalectomized rats than in control animals. These results suggest that the cellular transport systems involved in the endolymph secretion may be altered by different hormones such as antidiuretic hormone and/or adrenocorticosteroid hormones. Nevertheless, the hormonal modulation of the inner ear fluid homeostasis remains to be further documented.

Adrenal Cortex Hormones↗

PubMed1996

Effects of clofilium, a K channel blocker, on electrogenic K secretion and afferent discharge at the frog semicircular canal. A preliminary report.

Application of clofilium to the endolymphatic side of the isolated frog semicircular canal abolished the transepithelial potential and produced increased K and mannitol outfluxes from the lumen to the dark cells or the basolateral perilymph, with no apparent effect on active K secretion. These results suggest an increased permeability of the paracellular pathway. When applied to the perilymphatic side in the intact labyrinth, clofilium reduced the rates of quantal transmitter release (miniature EPSP frequency), an effect that might arise from a decrease in the transduction current intensity secondary to the reduced transepithelial electrochemical potential for K+. Moreover, afferent spike rates were almost completely abolished at rest as well as during mechanical stimulation. This effect together with a decreased mEPSP amplitude points to a further direct action of clofilium on the afferent postsynaptic terminal. These results suggest a multi-factorial effect of clofilium that would reduce the sensitivity of the vestibular function.

Animals↗

PubMed1996

Effect of glycerol on electrochemical composition of endolymph and perilymph in the rat.

Glycerol (2 g/kg body weight), or 0.15 M NaCl for control animals, was administered to rats by i.v. injection. The dose was chosen in order to obtain an osmolarity increase in plasma of about 15 mosm/l 1 h after the glycerol administration, an increase which is similar to that observed in the human glycerol dehydration test. Endolymph and perilymph were sampled from the basal turn of the cochlea; cerebrospinal fluid (CSF) was sampled from cisterna magna. Plasma osmolarity, endocochlear potential, Na and K concentrations in endolymph, perilymph and CSF were determined 1 and 2 h after the glycerol injection. Compared with control animals, glycerol induced an increase in Na and K concentration in perilymph and endolymph, respectively, 1 and 2 h after the glycerol injection. No modification of the endocochlear potential was observed. These results are compatible with an increase in inner ear fluids osmolarity induced by glycerol.

Action Potentials↗

PubMed1995

Effect of cisplatin administration on the electrochemical composition of endolymph in the rat cochlea.

The effect of cisplatin on the electrochemical composition of the cochlear endolymph was studied in Long-Evans rats three days after a single intraperitoneal injection (8 mg/kg b.w.). A dose 2/3 of LD50 induced a decrease of the endolymphatic concentration of potassium whereas the endocochlear potential was unaffected. The discrepancy between these two findings indicated that cisplatin did not alter the mechanisms involved in the genesis of the endocochlear potential but modified the passive K transport into endolymph.

Analysis of Variance↗

PubMed1995

Comparative entry of carboplatin and sucrose in endolymph in the rat cochlea.

The permeability of the perilymphatic-endolymphatic interface for carboplatin was determined after lateral cerebral ventricle infusion of radioactive carboplatin (cis-diamine[1,1-cyclobutane-1-14C-dicarboxylate]platinum) to rats. [14C]sucrose, a similar weight molecule was used for comparison of the kinetics in the inner ear fluids. 14C-radioactivity was measured in perilymph and endolymph. The rate of elimination of the tracers from perilymph was equivalent indicating no difference in transport across the blood-perilymph barrier. The transport from perilymph to endolymph was very restricted for both substances. The present study indicates that the ototoxic effect of carboplatin cannot be explained by a specific endolymphatic transport mechanism.

Animals↗

PubMed1995

In vitro electrogenic K secretion in the frog semicircular canal: absence of effect of streptomycin.

In vitro, the frog semicircular canal secretes an endolymph-like fluid, i.e. a K-rich, positively polarized fluid. This electrogenic K secretion involved basolateral Na+, K(+)-ATPase and Na-K-Cl co-transporter and a luminal protein possessing sulfhydryl groups blocked by N-ethylmaleimide. Streptomycin, an ototoxic antibiotic, is known to block the non-specific mechano-dependent channels in the sensory cells of the ampulla of the semicircular canal. The aim of the present study was to investigate the possible effect of streptomycin on the K fluxes in the ampulla of the semicircular canal. The posterior frog semicircular canal was isolated and the lumen was filled with perilymph-like solution containing or not containing 0.5 mM streptomycin. The luminal K concentration and the transepithelial potential were measured and the unidirectional K fluxes calculated. The K influxes (into the lumen, pmoles/min/mm2) were 114 +/- 25.9 and 111 +/- 3.2 (mean +/- SE, n = 3) in the absence and presence of streptomycin, respectively. The transepithelial potential was not altered (4.0 +/- 1.08 mV versus 3.4 +/- 1.03 mV, n = 3). When ouabain (10(-3)M) was added to the basolateral solution together with luminal streptomycin, no further alteration occurred as compared with the effect of ouabain alone. These results suggest that in these conditions, the sensory organ does not have a major role in the endolymphatic K secretion in the ampulla of the frog semicircular canal.

Animals↗

PubMed1994

Antidiuretic hormone restores the endolymphatic longitudinal K+ gradient in the Brattleboro rat cochlea.

In the cochlea, endolymph is hyperosmotic to plasma and perilymph. To test the hypothesis that antidiuretic hormone is involved in the modulation of endolymph secretion, the electrochemical composition of cochlear fluids, endolymph and perilymph, was studied in three groups of anaesthetized rats: control Long Evans rats, homozygous Brattleboro rats that are genetically deprived of antidiuretic hormone, and Brattleboro rats that were treated with antidiuretic hormone (dDAVP, 0.5 microgram/100 g body weight/24 h during 8 days). Endolymph was sampled from the scala media at each turn of the cochlea and perilymph from the scala vestibuli. In Long Evans rats, the endocochlear potential, the endolymphatic K+ and Cl- concentrations decreased from base to apex of the cochlea as previously reported in guinea pigs and Sprague Dawley rats. In Brattleboro rats, the endocochlear potential and the Cl- concentration gradients were still present, whereas the K+ concentration gradient were still present, whereas the K+ concentration gradient was absent. This K+ gradient was restored by the administration of dDAVP, which increased the K+ concentration at the base of the cochlea. This work indicates that the K+ secretion in endolymph, and thus the osmolality, may be locally modulated by the antidiuretic hormone, probably via V2 receptors.

Animals↗

PubMed1993

N-ethylmaleimide-inhibited electrogenic K+ secretion in the ampulla of the frog semicircular canal.

1. The mechanisms of K+ secretion into endolymph were studied on a preparation of isolated semicircular canal with different pharmacological inhibitors. Three periods of 5 or 30 min were performed, the first as control, the second in the presence of the drugs added to the apical or the basolateral bathing solution, and the third as recovery. Apical fluid was sampled at the beginning and the end of each period, transepithelial potential was recorded, Na+, K+, and Cl- concentrations, and K+ efflux, with 86Rb+ as a tracer, were measured and K+ fluxes were calculated. 2. When both sides of the epithelium were bathed with perilymph-like solution, the epithelium absorbed Na+, secreted K+, and generated a lumen positive potential. 3. The ATPases inhibitors, ouabain (10(-5) and 10(-3) M) and N-ethylmaleimide (10(-4) and 10(-3) M) inhibited the electrogenic K+ secretion when added to the basolateral fluid. N-ethylmaleimide (10(-3) M) applied to the apical fluid during a 5 min period decreased the K+ influx by 43% and the transepithelial potential by 66%. Other ATPase inhibitors, harmaline (10(-3) M), omeprazole (10(-4) M), vanadate (10(-4) M and 10(-3) M), N,N'-dicyclohexylcarbodiimide (DCC, 10(-5) M), 7-chloro-4-nitrobenz-2-oxa-1,3-diazole (NBD-Cl, 5 x 10(-6) M and 5 x 10(-5) M), and bafilomycin (10(-7) M) did not affect the K+ transport nor the transepithelial potential when they were added to the apical fluid. 4. The Na(+)-K(+)-Cl- co-transporter inhibitor, bumetanide, decreased both the transepithelial potential and the K+ transport when added to the basolateral solution but not to the apical one. At 10(-6) M, bumetanide maximally decreased the K+ influx by about 60%. 5. K+ channel blockers, quinine (10(-4) M), TEA (5 x 10(-3) M), added to the apical solution and barium (2 x 10(-3) M) added to either the apical or the basolateral solutions, did not affect the K+ transport and the transepithelial potential. 6. The carbonic anhydrase inhibitor acetazolamide (10(-3) M) added to both apical and basolateral solutions did not affect the K+ transport and the transepithelial potential. 7. It is concluded that, in the ampulla of the semicircular canal, a basolateral Na(+)-K(+)-Cl- co-transporter energized by the Na+, K(+)-ATPase was involved for 60% in the K+ secretion into endolymph. The electrogenic K+ transport would partly depend on a N-ethylmaleimide-sensitive protein possibly located at the apical plasma membrane or intracellularly.

Animals↗

PubMed1993

Is the endolymphatic K secretion electrogenic?

The endolymphatic potential is assumed to result from active K transport into the endolymphatic compartment and passive K diffusion in the opposite direction. However, in several in vivo experiments, changes in the endolymphatic potential differed from those in the endolymphatic K concentration. Moreover, in in vitro experiments, a negative endolymphatic potential was observed in the presence of ouabain without K gradient between the two compartments. These observations suggest that the coupling between the K transport and the genesis of the endolymphatic potential is not tight. Several factors may separately influence the endolymphatic potential and the K transport such as the acid-base equilibrium, the integrity of Reissner's membrane, the hormonal status, and the Na transport.

Animals↗