Shennan D B
Hannah Research Institute, Scotland.
Q J Exp Physiol. 1989 Nov;74(6):927-38. doi: 10.1113/expphysiol.1989.sp003363.
The transport of K+ (using 86Rb as tracer) by lactating rat mammary tissue slices has been studied in order to seek evidence for Na+-K+-Cl- co-transport. Potassium transport was inhibited by furosemide; the locus of inhibition was at a site other than the Na+:K+ pump. Replacing medium Cl- with NO3 reduced the bidirectional movement of K+; moreover, furosemide was without effect in a Cl- -free medium. Sodium replacement by N-methyl-D-glucamine acted to reduce the loop diuretic-sensitive component of K+ uptake whilst concomitantly increasing K+ influx via an ouabain- and furosemide-resistant pathway. Potassium efflux was found to be transiently stimulated by Na+ ions; this was attenuated by furosemide. Potassium egress was markedly increased via a furosemide-insensitive pathway when salicylate was used to replace Cl-. The results are consistent with furosemide-sensitive Na+-K+-Cl- co-transport.
为了寻找Na⁺-K⁺-Cl⁻协同转运的证据,研究了用⁸⁶Rb作为示踪剂时泌乳大鼠乳腺组织切片对K⁺的转运。呋塞米抑制钾的转运;抑制位点在Na⁺:K⁺泵以外的部位。用NO₃取代培养基中的Cl⁻会降低K⁺的双向移动;此外,呋塞米在无Cl⁻的培养基中无效。用N-甲基-D-葡萄糖胺取代钠可降低K⁺摄取中对袢利尿剂敏感的成分,同时通过哇巴因和呋塞米耐药途径增加K⁺内流。发现钾外流受到Na⁺离子的短暂刺激;这被呋塞米减弱。当用水杨酸盐取代Cl⁻时,钾外流通过呋塞米不敏感的途径显著增加。结果与呋塞米敏感的Na⁺-K⁺-Cl⁻协同转运一致。