External Ni2+ and ENaC in A6 cells: Na+ current stimulation by competition at a binding site for amiloride and Na+

Autor(en): Cucu, D
Simaels, J
Van Driessche, W
Zeiske, W
Stichwörter: A6 cells; ALPHA-SUBUNIT; APICAL MEMBRANE; Biochemistry & Molecular Biology; Cell Biology; CHANNEL DENSITY; CHEMICAL-STIMULATION; CONCENTRATION-DEPENDENCE; CURRENT FLUCTUATIONS; ENaC; FROG-SKIN; Ni2+; noise analysis; Physiology; self-inhibition; SODIUM ENTRY; TRANSEPITHELIAL CAPACITANCE; XENOPUS-LAEVIS
Erscheinungsdatum: 2003
Herausgeber: SPRINGER
Journal: JOURNAL OF MEMBRANE BIOLOGY
Volumen: 194
Ausgabe: 1
Startseite: 33
Seitenende: 45
Zusammenfassung: 
In cultured A6 monolayers from distal Xenopus kidney, external Ni2+ stimulated active Na+ uptake via the epithelial Na+ channel, ENaC. Transepithelial capacitance measurements ruled out exocytosis of ENaC-containing vesicles underlying the Ni2+ effect. Na+ current noise analysis was performed using the neutral Na+-channel blocker 6-chloro-3.5-diamino-pyrazine-2-carboxamide (CDPC) and amiloride. The analysis of CDPC-induced noise in terms of a three-state channel model revealed that Ni2+ elicits an increase in the number of open channels as well as in the spontaneous open probability. While Ni2+ had no influence on CDPC-blocker kinetics, the macroscopic and microscopic blocking kinetics of amiloride were affected. Ni2+ turned out to compete with amiloride for a putative binding site but not with CDPC. Moreover, external Na+-known to compete with amiloride and so producing the ``self-inhibition'' phenomenon-and Ni2+ exerted mutually exclusive analogous effects on amiloride kinetics. Na+ current kinetics revealed that Ni2+ prevents ENaC to be downregulated by self-inhibition. Co2+ behaved similarly to Ni2+, whereas Zn2+ did not. Attempts to disclose the chemical nature of the site reacting with Ni2+ suggested cysteine but not histidine as reaction partner.
ISSN: 00222631
DOI: 10.1007/s00232-003-2023-y

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