PMID- 8416943
OWN - NLM
STAT- MEDLINE
DCOM- 19930128
LR  - 20210210
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 268
IP  - 1
DP  - 1993 Jan 5
TI  - Roles of phospholipase C and Ca(2+)-ATPase in calcium responses of single, 
      fibrinogen-bound platelets.
PG  - 356-63
AB  - Fura-2-loaded platelets were immobilized on fibrinogen, and cytosolic free 
      calcium concentration ([Ca2+]i) was measured by video imaging of the fluorescence 
      signal. In the immobilized, single platelets, ADP and low doses of thrombin 
      evoked repetitive spikes of [Ca2+]i, whereas higher thrombin concentrations gave 
      elevated plateaus in [Ca2+]i. Stimulation of the cells with thrombin after the 
      addition of ADP changed the frequency of spiking, but not the maximal levels of 
      [Ca2+]i reached. In suspensions of platelets, ADP and low doses of thrombin 
      evoked transient elevation of myo-inositol phosphates, suggesting that the 
      initiation of spiking was due to stimulation of phospholipase C. In platelet 
      suspensions, the Ca(2+)-ATPase inhibitor thapsigargin (TG) evoked a gradual rise 
      in [Ca2+]i, which was potentiated by preactivation of the platelets and inhibited 
      by prostaglandin E1 and nitroprusside. In single platelets, TG induced a sudden 
      increase in [Ca2+]i after a long but variable delay, followed by a phase of slow 
      oscillations. The effects of preactivation with ADP were 2-fold: the delay time 
      before the response to TG was shortened and the maximal level of [Ca2+]i reached 
      with TG was higher than the level of the preceding Ca2+ spikes. Apparently, Ca2+ 
      responses induced by the inhibition of Ca(2+)-ATPases are potentiated by prior 
      elevation of [Ca2+]i and reduced by substances that inhibit agonist-evoked 
      increases in [Ca2+]i. The data point to a mechanism of Ca(2+)-induced Ca2+ 
      release and the presence of TG-sensitive and TG-insensitive Ca2+ stores in 
      platelets. Rapid spiking may involve both pools, whereas the latter alone may 
      account for the slow TG-evoked oscillations.
FAU - Heemskerk, J W
AU  - Heemskerk JW
AD  - Department of Biochemistry, University of Limburg, Maastricht, The Netherlands.
FAU - Vis, P
AU  - Vis P
FAU - Feijge, M A
AU  - Feijge MA
FAU - Hoyland, J
AU  - Hoyland J
FAU - Mason, W T
AU  - Mason WT
FAU - Sage, S O
AU  - Sage SO
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Inositol Phosphates)
RN  - 0 (Terpenes)
RN  - 526U7A2651 (Egtazic Acid)
RN  - 61D2G4IYVH (Adenosine Diphosphate)
RN  - 67526-95-8 (Thapsigargin)
RN  - 9001-32-5 (Fibrinogen)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - EC 3.4.21.5 (Thrombin)
RN  - EC 3.6.1.5 (Apyrase)
RN  - EC 7.2.2.10 (Calcium-Transporting ATPases)
RN  - R16CO5Y76E (Aspirin)
RN  - SY7Q814VUP (Calcium)
RN  - TSN3DL106G (Fura-2)
SB  - IM
MH  - Adenosine Diphosphate/pharmacology
MH  - Apyrase/pharmacology
MH  - Aspirin/pharmacology
MH  - Blood Platelets/drug effects/enzymology/*metabolism
MH  - Calcium/*blood
MH  - Calcium-Transporting ATPases/antagonists & inhibitors/*blood
MH  - Cytosol/metabolism
MH  - Egtazic Acid/pharmacology
MH  - Fibrinogen/*pharmacology
MH  - Fura-2
MH  - Humans
MH  - Inositol Phosphates/*blood
MH  - Kinetics
MH  - Platelet Activation
MH  - Spectrometry, Fluorescence
MH  - Terpenes/pharmacology
MH  - Thapsigargin
MH  - Thrombin/pharmacology
MH  - Type C Phospholipases/*blood
MH  - Video Recording
EDAT- 1993/01/05 00:00
MHDA- 1993/01/05 00:01
CRDT- 1993/01/05 00:00
PHST- 1993/01/05 00:00 [pubmed]
PHST- 1993/01/05 00:01 [medline]
PHST- 1993/01/05 00:00 [entrez]
AID - S0021-9258(18)54158-2 [pii]
PST - ppublish
SO  - J Biol Chem. 1993 Jan 5;268(1):356-63.