PMID- 2833660
OWN - NLM
STAT- MEDLINE
DCOM- 19880523
LR  - 20131121
IS  - 0023-6837 (Print)
IS  - 0023-6837 (Linking)
VI  - 58
IP  - 4
DP  - 1988 Apr
TI  - ATP induces transient elevations of [Ca2+]i in human neutrophils and primes these 
      cells for enhanced O2- generation.
PG  - 448-53
AB  - ATP, when added to human polymorphonuclear neutrophils (PMNs) at concentrations 
      similar to those attained extracellularly at sites of platelet thrombus formation 
      (0.1 to 20 microM), causes an enhancement of 
      N-formyl(methionyl)leucylphenylalanine (FMLP)-stimulated superoxide anion (O2-) 
      generation. However, ATP by itself is an ineffective agonist for O2- generation 
      by PMNs. The ATP-induced enhancement of O2- generation is associated with a 
      shortened lag time in the response of PMNs to FMLP without a change in the median 
      effective dose for FMLP, suggesting that signal transduction, rather than altered 
      receptor affinity, is responsible for the enhanced oxidative response. Maximum 
      enhancement of O2- generation is detected as early as 15 seconds and is 
      maintained for at least 10 minutes. Of various nucleotides and 
      nonhydrolyzable-ATP analogs test d, only ATP, UTP, and ITP were found to cause 
      enhanced O2- generation by PMNs. Addition of ATP to quin2-loaded PMNs, in the 
      absence of other stimuli, elicits a dramatic rise in [Ca2+]i which reaches a 
      maximum of 500 to 800 nM at 30 seconds and slowly returns to baseline over 5 
      minutes. This ATP-induced rise in intracellular free Ca2+ concentration is 
      correlated with the enhancement of FMLP-stimulated O2- generation both with 
      respect to dose and nucleotide specificity. Stimulated Ca2+ uptake, rather than 
      mobilization of intracellular Ca2+ stores, appears to be primarily responsible 
      for the rise in intracellular free Ca2+ concentration. These studies indicate 
      that an ATP-induced rise in intracellular free Ca2+ concentration, although 
      insufficient by itself to elicit O2- generation by PMNs, is associated with a 
      priming of PMNs for enhanced O2- generation when stimulated by other agonists.
FAU - Kuhns, D B
AU  - Kuhns DB
AD  - Department of Hematology, Walter Reed Army Institute of Research, Washington D.C.
FAU - Wright, D G
AU  - Wright DG
FAU - Nath, J
AU  - Nath J
FAU - Kaplan, S S
AU  - Kaplan SS
FAU - Basford, R E
AU  - Basford RE
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Lab Invest
JT  - Laboratory investigation; a journal of technical methods and pathology
JID - 0376617
RN  - 0 (Virulence Factors, Bordetella)
RN  - 11062-77-4 (Superoxides)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenosine Triphosphate/*pharmacology
MH  - Blood Platelets/physiology
MH  - Calcium/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Humans
MH  - N-Formylmethionine Leucyl-Phenylalanine/pharmacology
MH  - Neutrophils/*drug effects/metabolism
MH  - Superoxides/*metabolism
MH  - Virulence Factors, Bordetella/pharmacology
EDAT- 1988/04/01 00:00
MHDA- 1988/04/01 00:01
CRDT- 1988/04/01 00:00
PHST- 1988/04/01 00:00 [pubmed]
PHST- 1988/04/01 00:01 [medline]
PHST- 1988/04/01 00:00 [entrez]
PST - ppublish
SO  - Lab Invest. 1988 Apr;58(4):448-53.