Cation transport in the ampulla of the semicircular canal and in the endolymphatic sac

Abstract

We examined the effects of anoxia and ethacrynic acid on the endolymphatic potential and cation activity in the superior ampulla of the guinea pig, using double-barrelled ion-exchanger microelectrodes. In normal guinea pigs the ampullar endolymphatic potential was + 3.9 +/- 1.2 mV (n = 32), the Cl- activity 130 +/- 4.6 mM (n = 9), and the Na+ activity 18.4 +/- 4.4 mM (n = 20). After anoxia, the ampullar DC potential decreased rapidly and reversed its polarity within 5 min. It then decreased gradually for 60 min and increased afterwards to approximately zero. K+ activity decreased gradually after a latency of 10 min, whereas Na+ activity increased. During the gradual decrease of a negative ampullar endolymphatic potential, an increase in Na+ activity was observed. Thirty minutes after the intravenous injection of ethacrynic acid (100 mg/kg), the potential began to decrease, changed to a negative polarity, and approached a maximum negative level 100 min after the injection. The decrease in K+ activity corresponded to the reduction of potential whereas Na+ activity remained unchanged. The DC potential of the endolymphatic sac in normal guinea pigs was + 14.7 +/- 5.1 mV (n = 17). The Na+ concentration was 103.3 +/- 14.7 mM (n = 14) and the K+ concentration was 11.6 +/- 0.8 mM (n = 4). After anoxia, the DC potential decreased rapidly and approached 0 mV within 8 min. No negative potential could be observed. The Na+ concentration began to increase 2 min after anoxia and reached the extracellular Na+ concentration about 30 min later.(ABSTRACT TRUNCATED AT 250 WORDS)

Endolymphatic sac is involved in the regulation of hydrostatic pressure of cochlear endolymph

“…Ion transporters of sodium and/or chloride from the ES lumen to the outside are suggested to be present in ES epithelial cells (3,14,15,20 Catecholamines have also been reported to increase potassium secretion in marginal cells of the stria vascularis via ␤ 1 adrenergic actions (36). If isoproterenol changes endolymphatic pressure by increasing potassium secretion in marginal cells, EP would be increased with no influence of ES obstruction on the response of cochlear hydrostatic pressure to isoproterenol.…”

“…ES direct current potential (ESP) and endocochlear direct current potential (EP) are known to be present in the ES and the cochlea, respectively (3,12,15). ESP and EP are generated by active ion transports in the ES and cochlea, respectively (3,15,21).…”

“…ESP and EP are generated by active ion transports in the ES and cochlea, respectively (3,15,21). ESP and EP can thus be used as indices of function for the ES and cochlea, respectively (15,21).…”

Functional and Molecular Expression of Epithelial Sodium Channels in Cultured Human Endolymphatic Sac Epithelial Cells

“…Although the Na + concentration of cochlear endolymph is very low, the endocochlear potential (+80 mV) can serve as a sufficient electrical driving force for Na + movement through the ENaC, which may be involved in maintaining a low-Na + concentration in the endolymph. Interestingly, the composition of the luminal fluid in the ES differs from that in the cochlea; the K + concentration is lower (15 mmol/L), the Na + concentration is higher (100 mmol/L) (8). Therefore, if the ENaC is expressed in the apical membrane of ES epithelial cells, then Na + movement through the ENaC is a strong candidate as a regulator of fluid absorption in the ES epithelium.…”

Le sac endolymphatique : ses fonctions au sein de l’oreille interne

“…De plus, au cours des labyrinthites expérimentales d'origine immunitaire, le sac endolymphatique est la première structure de l'oreille interne infiltrée par des cellules inflammatoires, et sa destruction diminue considérablement les réactions immunitaires locales de l'oreille interne [19]. Enfin, Cette hypothèse est confirmée par la baisse de la concentration luminale de K + et l'augmentation de celle de Na + observées lors de l'inhibition des systèmes de transport actif au cours de l'anoxie [30]. Le Na + serait réab-sorbé par l'action conjuguée de transporteurs apicaux, cotransport Na-K-2Cl (inhibé par le bumétanide), échangeur Na + /H + (inhibé par l'amiloride) et canal Na de type ENaC (epithelial Na channel), et d'une Na + ,K + -ATPase basolatérale (inhibée par l'ouabaïne) [31][32][33][34][35].…”