PMID- 8864567
OWN - NLM
STAT- MEDLINE
DCOM- 19961216
LR  - 20190920
IS  - 0143-4160 (Print)
IS  - 0143-4160 (Linking)
VI  - 20
IP  - 1
DP  - 1996 Jul
TI  - Two different store-operated Ca2+ entry pathways in MDCK cells.
PG  - 11-9
AB  - Whole cell patch clamp experiments in conjunction with Fura-2 fluorescence 
      microscopy were performed to study the mechanisms of 'store-operated' 
      (capacitative) Ca2+ entry. In MDCK cells, depletion of inositol 
      1,4,5-trisphosphate (IP3)-sensitive Ca2+ stores activates a store-operated cation 
      current (SOCC) predominantly selective for Ca2+ than for Na+ or Mn2+ [Delles C., 
      Haller T., Dietl P. A highly calcium-selective cation current activated by 
      intracellular calcium release in MDCK cells. J Physiol 1995, 486: 557-569]. In 
      the presence of extracellular Ca2+, thapsigargin (TG) stimulated both SOCC and a 
      Ca(2+)-dependent K+ current (IK(Ca)), reflecting stimulation of store-operated 
      Ca2+ entry. The Ca2+ entry blocker 1-[3-(4-methoxyphenyl) 
      propoxyl]-1-(4-methoxyphenyl)-ethyl-1H-imidazole HCI (SK&F96365; 30 microM) did 
      not inhibit SOCC. At the same concentration, it exerted a transient partial 
      inhibition on IK(Ca) activated by TG-induced Ca2+ entry. It did, however, not 
      directly inhibit IK(Ca). This was demonstrated by an unchanged relationship 
      between the cytosolic Ca2+ concentration ([Ca2+]i) and IK(Ca) in experiments 
      where [Ca2+]i was measured under whole cell patch clamp conditions and by a 
      lacking effect of SK&F96365 on IK(Ca) prestimulated by a high 'clamped' [Ca2+]i. 
      La3+ partially, but not directly, inhibited the TG-induced IK(Ca) at a 
      concentration (10 microM) sufficient to entirely block SOCC. La3+ and SK&F96365 
      in combination exerted an additive reduction on the TG-induced whole cell 
      conductance (G) and completely blocked IK(Ca) stimulated by TG. We conclude that 
      two Ca2+ entry pathways with different pharmacological and biophysical properties 
      are involved in 'store-operated' Ca2+ entry in MDCK cells.
FAU - Dietl, P
AU  - Dietl P
AD  - Department of Physiology, University of Innsbruck, Austria. paul.dietl@ulbk.ac.at
FAU - Haller, T
AU  - Haller T
FAU - Wirleitner, B
AU  - Wirleitner B
FAU - Friedrich, F
AU  - Friedrich F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Cell Calcium
JT  - Cell calcium
JID - 8006226
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Calcium Channels)
RN  - 0 (Imidazoles)
RN  - 0 (Potassium Channels)
RN  - 67526-95-8 (Thapsigargin)
RN  - 6I3K30563S (Lanthanum)
RN  - 85166-31-0 (Inositol 1,4,5-Trisphosphate)
RN  - I61V87164A (1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole)
SB  - IM
MH  - Animals
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium Channels/drug effects/*physiology
MH  - Cells, Cultured/*metabolism
MH  - Dogs
MH  - Electric Conductivity
MH  - Imidazoles/pharmacology
MH  - Inositol 1,4,5-Trisphosphate/pharmacology
MH  - Lanthanum/pharmacology
MH  - Potassium Channels/drug effects/physiology
MH  - Thapsigargin/pharmacology
EDAT- 1996/07/01 00:00
MHDA- 1996/07/01 00:01
CRDT- 1996/07/01 00:00
PHST- 1996/07/01 00:00 [pubmed]
PHST- 1996/07/01 00:01 [medline]
PHST- 1996/07/01 00:00 [entrez]
AID - S0143-4160(96)90046-9 [pii]
AID - 10.1016/s0143-4160(96)90046-9 [doi]
PST - ppublish
SO  - Cell Calcium. 1996 Jul;20(1):11-9. doi: 10.1016/s0143-4160(96)90046-9.