PMID- 2096220
OWN - NLM
STAT- MEDLINE
DCOM- 19910717
LR  - 20191029
IS  - 0887-2082 (Print)
IS  - 0887-2082 (Linking)
VI  - 5
IP  - 4
DP  - 1990 Winter
TI  - Oxidant injury increases cell surface receptor binding of angiotensin II to 
      pulmonary artery endothelial cells.
PG  - 253-8
AB  - Nitrogen dioxide (NO2), an environmental oxidant, is known to activate 
      phospholipase A1 and modulate the plasma membrane structure of porcine pulmonary 
      artery endothelial cells. We evaluated the effects of exposure to NO2, purified 
      phospholipase B (which acts as phospholipase A1 and A2), or phospholipase A2 on 
      125I-angiotensin II (Ang II) receptor binding, internalization, or both in 
      pulmonary endothelial cells. Exposure to 5 ppm NO2 for 48 hr at 37 degrees C or 
      0.075 U each of phospholipase B or A2 in phosphate-buffered saline (PBS) for 30 
      min at 24 degrees C resulted in an increase in total Ang II binding (i.e., cell 
      surface bound and internalized) by 45% (p less than 0.05), 50% (p less than 
      0.05), and 85% (p less than 0.001), respectively, compared to controls. An Ang II 
      receptor antagonist, [Sar1 Ile8] Ang II, competitively displaced Ang II binding 
      to control, NO2-, phospholipase B-, and phospholipase A2-exposed cells. 
      Dissociation of bound Ang II in the presence of PBS was less than 1% of total 
      bound Ang II in control, NO2-, and phospholipase B-exposed cells and was 50% of 
      total bound Ang II in phospholipase A2-exposed cells. In the presence of isotonic 
      acetic acid/NaCl, in excess of 90% of cell surface-bound Ang II was dissociated 
      from control, NO2-, and phospholipase B-exposed cells, and there was less than 2% 
      of Ang II detectable when acid-treated cells were subjected to NaOH 
      solubilization. In cells exposed to phospholipase A2, acetic acid treatment did 
      not release cell-bound Ang II, and the remaining Ang II was recovered in the NaOH 
      solubilized fraction.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Patel, J M
AU  - Patel JM
AD  - Division of Pulmonary Medicine, University of Florida College of Medicine, 
      Gainesville 32608-1197.
FAU - Sekharam, K M
AU  - Sekharam KM
FAU - Block, E R
AU  - Block ER
LA  - eng
GR  - ES03989/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Biochem Toxicol
JT  - Journal of biochemical toxicology
JID - 8700114
RN  - 0 (Environmental Pollutants)
RN  - 0 (Iodine Radioisotopes)
RN  - 0 (Receptors, Angiotensin)
RN  - 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II)
RN  - EC 3.1.1.32 (Phospholipases A)
RN  - EC 3.1.1.32 (Phospholipases A1)
RN  - EC 3.1.1.4 (Phospholipases A2)
RN  - EC 3.1.1.5 (Lysophospholipase)
RN  - S7G510RUBH (Nitrogen Dioxide)
SB  - IM
MH  - 1-Sarcosine-8-Isoleucine Angiotensin II/metabolism
MH  - Animals
MH  - Binding, Competitive
MH  - Cell Membrane/drug effects/metabolism
MH  - Cells, Cultured
MH  - Endothelium, Vascular/cytology/*drug effects
MH  - Environmental Pollutants/*toxicity
MH  - Iodine Radioisotopes
MH  - Lysophospholipase/*metabolism
MH  - Nitrogen Dioxide/*toxicity
MH  - Phospholipases A/*metabolism
MH  - Phospholipases A1
MH  - Phospholipases A2
MH  - Pulmonary Artery/cytology/drug effects
MH  - Receptors, Angiotensin/*drug effects
MH  - Swine
EDAT- 1990/01/01 00:00
MHDA- 1990/01/01 00:01
CRDT- 1990/01/01 00:00
PHST- 1990/01/01 00:00 [pubmed]
PHST- 1990/01/01 00:01 [medline]
PHST- 1990/01/01 00:00 [entrez]
AID - 10.1002/jbt.2570050408 [doi]
PST - ppublish
SO  - J Biochem Toxicol. 1990 Winter;5(4):253-8. doi: 10.1002/jbt.2570050408.