Dependence of endocochlear potential on basolateral Na+ and Cl- concentration: a study using vascular and perilymph perfusion.
Inside-positive endocochlear potential (EP) and high potassium concentration in the endocochlear duct are generated by transepithelial K+ transport in marginal cells of the stria vascularis. In order to estimate the degree of involvement of Na+ and Cl- in K+ transport in marginal cells, EP in guinea pigs was measured under artificial vascular and perilymphatic perfusion in situ. Na+ depletion due to both vascular and perilymphatic perfusion decreased EP by -10.0 +/- 4.1 mV (delta EP = -86 +/- 5.2 mV, n = 5) from the control value of 78 +/- 4.3 mV (p < 0.01). Cl- depletion due to vascular and perilymphatic perfusion also decreased EP by -10.0 +/- 4.9 mV (delta EP = 8.5 +/- 4.8 mV, n = 6) from the control value of 77 +/- 5.1 mV (p < 0.01). However, under either vascular or perilymphatic perfusion, even lowering of Na+ or Cl- concentration in the perfusate decreased EP only slightly compared to the results under both vascular and perilymphatic perfusion. Furosemide, a blocker of Na+/K+/2Cl- symport, decreased EP under vascular perfusion. This dependency of EP on basolateral Na+ and Cl- concentration strongly suggests that K+ transport by the marginal cell is dependent on the basolateral Na+ and Cl- concentration, and that Na+/K+/2Cl- symport is raised as a possible mechanism for Na+ and Cl- dependency of EP.
Shindo
M
M
Department of Otorhinolaryngology, Kyoto Prefectural Medical University, Japan.
Miyamoto
M
M
Abe
N
N
Shida
S
S
Murakami
Y
Y
Imai
Y
Y
D000818:Animals; D001485:Basement Membrane / Q000187:drug effects / Q000502:physiology; D001693:Biological Transport, Active / Q000187:drug effects; D002712:Chlorides / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000502:physiology*; D003051:Cochlea / Q000098:blood supply* / Q000502:physiology*; D003055:Cochlear Microphonic Potentials / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006168:Guinea Pigs; D010455:Peptides / Q000494:pharmacology; D010477:Perfusion; D010498:Perilymph / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000502:physiology*
D002712:Chlorides; D010455:Peptides; C029311:serum sodium transport inhibitor; D012964:Sodium; D011188:Potassium