PMID- 7473219
OWN - NLM
STAT- MEDLINE
DCOM- 19951212
LR  - 20190512
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 486 ( Pt 3)
IP  - Pt 3
DP  - 1995 Aug 1
TI  - A highly calcium-selective cation current activated by intracellular calcium 
      release in MDCK cells.
PG  - 557-69
AB  - 1. The whole-cell patch clamp technique and fluorescence microscopy with the Ca2+ 
      indicators fura-2 and fluo-3 were used to measure the whole-cell current and the 
      free intracellular Ca2+ concentration ([Ca2+]i) in Madin-Darby canine kidney 
      (MDCK) cells. 2. In a Ca(2+)-free bath solution, thapsigargin (TG) caused a 
      transient increase of [Ca2+]i. Subsequent addition of Ca2+ caused a long lasting 
      elevation of [Ca2+]i. 3. In a Ca(2+)-free bath solution, extracellular 
      application of TG, ATP or ionomycin, or intracellular application of inositol 
      1,4,5-trisphosphate (IP3), caused a small but significant inward current (Iin) 
      and a transient outward Ca(2+)-dependent K+ current (IK(Ca)), consistent with 
      intracellular Ca2+ release. Subsequent addition of Ca2+ induced a prominent Iin 
      with a current density of -4.2 +/- 0.7 pA pF-1. This Iin was unaffected by 
      inositol 1,3,4,5-tetrakisphosphate (IP4). 4. Na+ replacement by mannitol, 
      N-methyl-D-glucamine+ (NMG+), aminomethylidin-trimethanol+ (Tris+) or choline+ 
      reduced Iin by 54, 65, 52 and 56%, respectively. This indicates an apparent Ca2+ 
      selectivity over Na+ of 26:1. Iin was, however, unaffected by replacing Cl- with 
      gluconate- or by the K+ channel blocker charybdotoxin (CTX). 5. Iin was 
      completely blocked by La3+ (IC50 = 0.77 microM). Consistently, La3+ completely 
      reversed the TG-induced elevation of [Ca2+]i. SK&F 96365 
      (1-[3-(4-methoxyphenyl)-propoxyl]-1-(4-methoxy-phenyl)-ethyl-1H-im idazole) HCl 
      did not inhibit the TG-induced Iin. It did, however, exhibit a biphasic effect on 
      [Ca2+]i, consisting of an initial Ca2+ decay and a subsequent Ca2+ elevation. 
      La3+ completely reversed the SK&F 96365-induced elevation of [Ca2+]i. 6. In the 
      absence of Na+, Iin was dependent on the bath Ca2+ concentration (EC50 = 1.02 
      mM). Ca2+ replacement by Ba2+ or Mn2+ resulted in a reduction of Iin by 95 and 
      94%, respectively. 7. From these experiments we conclude that Ca2+ release from 
      intracellular Ca2+ stores, induced by different independent methods, stimulates 
      La(3+)-inhibitable Ca2+ entry in MDCK cells. Ca2+ entry is at least, in part, 
      mediated by a cation current, which is highly, but not exclusively, selective for 
      Ca2+ over Na+ and insensitive to SK&F 96365.
FAU - Delles, C
AU  - Delles C
AD  - Department of Physiology, University of Innsbruck, Austria.
FAU - Haller, T
AU  - Haller T
FAU - Dietl, P
AU  - Dietl P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Calcium Channels)
RN  - 0 (Cations)
RN  - 0 (Imidazoles)
RN  - 0 (Ionophores)
RN  - 56092-81-0 (Ionomycin)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - I61V87164A (1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole)
RN  - SY7Q814VUP (Calcium)
RN  - TSN3DL106G (Fura-2)
SB  - IM
MH  - Adenosine Triphosphate/pharmacology
MH  - Animals
MH  - Calcium/*physiology
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium Channels/drug effects/*metabolism
MH  - Cations/pharmacology
MH  - Cell Line
MH  - Dogs
MH  - Epithelial Cells
MH  - Epithelium/drug effects/metabolism
MH  - Fura-2
MH  - Imidazoles/pharmacology
MH  - Ionomycin/pharmacology
MH  - Ionophores/pharmacology
MH  - Kidney/*metabolism
MH  - Patch-Clamp Techniques
PMC - PMC1156546
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
PMCR- 1995/08/01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
PHST- 1995/08/01 00:00 [pmc-release]
AID - 10.1113/jphysiol.1995.sp020834 [doi]
PST - ppublish
SO  - J Physiol. 1995 Aug 1;486 ( Pt 3)(Pt 3):557-69. doi: 
      10.1113/jphysiol.1995.sp020834.