PMID- 7741761
OWN - NLM
STAT- MEDLINE
DCOM- 19950602
LR  - 20190623
IS  - 0006-2952 (Print)
IS  - 0006-2952 (Linking)
VI  - 49
IP  - 7
DP  - 1995 Mar 30
TI  - Refilling state of internal Ca2+ stores is not the only intracellular signal 
      stimulating Ca2+ influx in human endothelial cells.
PG  - 893-9
AB  - To further analyse the role of the refilling state of internal Ca2+ pools in the 
      stimulation of Ca2+ influx in human endothelial cells, we investigated the 
      combined effect of thapsigargin (TG) and histamine on cytosolic Ca2+ 
      concentration ([Ca2+]i) and inositol polyphosphate production. At normal 
      extracellular Ca2+ levels, TG induced a progressive and sustained elevation in 
      [Ca2+]i which was dose-dependently prevented by pretreatment with 1-10 microM 
      histamine. Similarly, pretreatment with 0.1 and 1 microM TG suppressed 
      histamine-induced Ca2+ transients partially and totally, respectively. TG 
      pretreatment did not alter the inositol triphosphate (IP3) level liberated by 
      histamine, but modified IP3 metabolism by decreasing inositol biphosphate (IP2) 
      and increasing inositol monophosphate (IP1) contents. In the absence of Ca2+ 
      influx, 1 microM TG only induced a small transient increase in [Ca2+]i whereas 
      the Ca2+ mobilization evoked by 10 microM histamine was unchanged. In both cases, 
      the absence of any additional effect of either TG, histamine or 2 microM 
      ionomycin indicated the complete depletion of Ca2+ stores. The re-establishment 
      of the transmembrane Ca2+ gradient induced a transient rise in [Ca2+]i. Its 
      amplitude differed between histamine- and TG-treated cells. It was imposed by 
      cell pretreatment and was selectively affected by changes in the membrane 
      potential. At 5 mM external K+, the transient rise in [Ca2+]i was more marked in 
      histamine- than in TG-stimulated cells; this difference was suppressed by TG 
      pretreatment. The presence of 130 mM external K+ increased Ca2+ entry in 
      TG-treated cells but reduced it in histamine-stimulated cells. These results 
      indicate that the refilling state of internal Ca2+ stores does not constitute the 
      single regulator of Ca2+ influx. TG and histamine seem to activate Ca2+ influx 
      through distinct but interdependent pathways regulated by membrane potential.
FAU - Iouzalen, L
AU  - Iouzalen L
AD  - Department of Pharmacology, Centre National de la Recherche Scientifique, 
      Universite Paris V, Necker's Medical School, France.
FAU - David-Dufilho, M
AU  - David-Dufilho M
FAU - Devynck, M A
AU  - Devynck MA
LA  - eng
PT  - Journal Article
PL  - England
TA  - Biochem Pharmacol
JT  - Biochemical pharmacology
JID - 0101032
RN  - 0 (Inositol Phosphates)
RN  - 0 (Terpenes)
RN  - 67526-95-8 (Thapsigargin)
RN  - 820484N8I3 (Histamine)
RN  - RWP5GA015D (Potassium)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Calcium/*metabolism
MH  - Cells, Cultured
MH  - Endothelium, Vascular/drug effects/*metabolism
MH  - Histamine/pharmacology
MH  - Humans
MH  - Inositol Phosphates/metabolism
MH  - Potassium/pharmacology
MH  - Signal Transduction
MH  - Terpenes/pharmacology
MH  - Thapsigargin
EDAT- 1995/03/30 00:00
MHDA- 1995/03/30 00:01
CRDT- 1995/03/30 00:00
PHST- 1995/03/30 00:00 [pubmed]
PHST- 1995/03/30 00:01 [medline]
PHST- 1995/03/30 00:00 [entrez]
AID - 0006-2952(94)00513-L [pii]
AID - 10.1016/0006-2952(94)00513-l [doi]
PST - ppublish
SO  - Biochem Pharmacol. 1995 Mar 30;49(7):893-9. doi: 10.1016/0006-2952(94)00513-l.