Shindo M, Miyamoto M, Abe N, Shida S, Murakami Y, Imai Y
Department of Otorhinolaryngology, Kyoto Prefectural Medical University, Japan.
Jpn J Physiol. 1992;42(4):617-30. doi: 10.2170/jjphysiol.42.617.
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.
内淋巴囊电位(EP)呈阳性以及内淋巴导管中高钾浓度是由血管纹边缘细胞的跨上皮钾离子转运产生的。为了评估钠离子和氯离子在边缘细胞钾离子转运中的参与程度,在原位人工血管和外淋巴灌注条件下测量了豚鼠的EP。血管和外淋巴灌注导致的钠离子缺失使EP从78±4.3mV的对照值下降了-10.0±4.1mV(δEP=-86±5.2mV,n=5)(p<0.01)。血管和外淋巴灌注导致的氯离子缺失也使EP从77±5.1mV的对照值下降了-10.0±4.9mV(δEP=8.5±4.8mV,n=6)(p<0.01)。然而,在血管或外淋巴灌注条件下,与血管和外淋巴联合灌注的结果相比,即使灌注液中钠离子或氯离子浓度降低,EP也只是略有下降。呋塞米是一种钠/钾/2氯同向转运体阻滞剂,在血管灌注时会降低EP。EP对基底外侧钠离子和氯离子浓度的这种依赖性强烈表明,边缘细胞的钾离子转运依赖于基底外侧钠离子和氯离子浓度,并且钠/钾/2氯同向转运被提出作为EP对钠离子和氯离子依赖性的一种可能机制。