多栉蚁（Formica polyctena）马尔皮基氏小管基底膜钾离子摄取机制：离子和抑制剂的作用

Mechanisms of K+ uptake across the basal membrane of malpighian tubules of Formica polyctena: the effect of ions and inhibitors.

作者信息

Leyssens A, Dijkstra S, Van Kerkhove E, Steels P

机构信息

Laboratory of Physiology, Limburgs Universitair Centrum, Diepenbeek, Belgium.

出版信息

J Exp Biol. 1994 Oct;195:123-45. doi: 10.1242/jeb.195.1.123.

DOI:10.1242/jeb.195.1.123

PMID:7964409

Abstract

In the presence of 6 mmol l-1 Ba2+, known to block the K+ channels in the basal membrane, a rise in bath [K+] ([K+]bl) induced an increase in intracellular K+ concentration ([K+]i) similar in amount and in time course to that obtained in the absence of Ba2+. The presence of active and passive (other than through K+ channels) K+ uptake mechanisms across the basal membrane was investigated in different bath K+ concentrations. Dihydro-ouabain (10(-3) mol l-1), a blocker of the Na+/K(+)-ATPase, tested in low bath [K+], and Sch28080 (10(-4) mol l-1), a K+/H(+)-ATPase inhibitor, were without effect on fluid secretion. Dihydro-ouabain was also without effect on electrical potential differences either in the absence or in the presence of Ba2+. Vanadate (10(-3) mol l-1), in contrast, strongly reduced fluid secretion not only in control solution but also in high-K+, Na(+)-free medium and reduced the transepithelial and the apical membrane potential differences but not the basal membrane potential difference of [K+]i. Omitting Na+ from the bathing medium, replacing Cl- by Br- or applying bumetanide (10(-5) mol l-1) inhibited fluid secretion only in a low-K+ (10 mmol l-1) medium. In 51 mmol l-1 [K+]bl, omitting Na+ was without effect and 10(-4) mol l-1 bumetanide was needed to inhibit secretion. Replacing Cl- by Br- stimulated fluid secretion at this K+ concentration. Bumetanide (10(-4) mol l-1) had no effect in 113 mmol l-1 [K+]bl. Bumetanide (10(-4) mol l-1) in 51 mmol l-1 [K+]bl did not affect membrane potentials, did not lower [K+]i and did not affect the rise in [K+]i observed on an increase in [K+]bl. The results were summarized in a model proposing that K+ channels play a dominant role in high-K+ (113 mmol l-1) bathing medium. A K+/Cl- cotransporter may become more important in 51 mmol l-1 [K+]bl and a K+/Na+/2Cl- cotransporter may gain in importance in 10 mmol l-1 [K+]bl. Active mechanisms for K+ uptake across the basal membrane seem to play no detectable role in sustaining fluid secretion. The response to vanadate might be due to an effect on the apical electrogenic H+ pump.

摘要

已知6 mmol l⁻¹ 的Ba²⁺ 可阻断基底膜中的钾通道，在此条件下，浴液中[K⁺]（[K⁺]bl）升高会诱导细胞内钾离子浓度（[K⁺]i）增加，其增加的幅度和时间进程与无Ba²⁺ 时相似。在不同的浴液钾浓度下，研究了跨越基底膜的主动和被动（除通过钾通道外）钾摄取机制。在低浴液[K⁺]条件下测试的钠钾ATP酶阻断剂二氢哇巴因（10⁻³ mol l⁻¹）和钾氢ATP酶抑制剂Sch28080（10⁻⁴ mol l⁻¹）对液体分泌均无影响。无论有无Ba²⁺，二氢哇巴因对电位差也均无影响。相比之下，钒酸盐（10⁻³ mol l⁻¹）不仅在对照溶液中，而且在高钾、无钠培养基中均强烈降低液体分泌，并降低跨上皮电位差和顶端膜电位差，但不影响[K⁺]i的基底膜电位差。从浴液培养基中去除Na⁺、用Br⁻ 替代Cl⁻ 或应用布美他尼（10⁻⁵ mol l⁻¹）仅在低钾（10 mmol l⁻¹）培养基中抑制液体分泌。在51 mmol l⁻¹ [K⁺]bl时，去除Na⁺ 无影响，需要10⁻⁴ mol l⁻¹ 的布美他尼来抑制分泌。在此钾浓度下，用Br⁻ 替代Cl⁻ 可刺激液体分泌。布美他尼（10⁻⁴ mol l⁻¹）在113 mmol l⁻¹ [K⁺]bl时无作用。51 mmol l⁻¹ [K⁺]bl时的布美他尼（10⁻⁴ mol l⁻¹）不影响膜电位，不降低[K⁺]i，也不影响[K⁺]bl升高时观察到的[K⁺]i升高。结果总结在一个模型中，该模型提出钾通道在高钾（113 mmol l⁻¹）浴液培养基中起主导作用。钾氯共转运体在51 mmol l⁻¹ [K⁺]bl时可能变得更重要，钾钠氯共转运体在10 mmol l⁻¹ [K⁺]bl时可能变得更重要。跨越基底膜的钾摄取主动机制似乎在维持液体分泌中不起可检测到的作用。对钒酸盐的反应可能是由于对顶端生电氢离子泵的影响。