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2015 ; 65
(4
): 784-92
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Cytosolic phospholipase A2? is critical for angiotensin II-induced hypertension
and associated cardiovascular pathophysiology
#MMPMID25667212
Khan NS
; Song CY
; Jennings BL
; Estes AM
; Fang XR
; Bonventre JV
; Malik KU
Hypertension
2015[Apr]; 65
(4
): 784-92
PMID25667212
show ga
Angiotensin II activates cytosolic phospholipase A(2)? (cPLA2?) and releases
arachidonic acid from tissue phospholipids, which mediate or modulate ?1
cardiovascular effects of angiotensin II and has been implicated in hypertension.
Because arachidonic acid release is the rate limiting step in eicosanoid
production, cPLA2? might play a central role in the development of angiotensin
II-induced hypertension. To test this hypothesis, we investigated the effect of
angiotensin II infusion for 13 days by micro-osmotic pumps on systolic blood
pressure and associated pathogenesis in wild type (cPLA2?(+/+)) and cPLA2?(-/-)
mice. Angiotensin II-induced increase in systolic blood pressure in cPLA2?(+/+)
mice was abolished in cPLA2?(-/-) mice; increased systolic blood pressure was
also abolished by the arachidonic acid metabolism inhibitor,
5,8,11,14-eicosatetraynoic acid in cPLA2?(+/+) mice. Angiotensin II in
cPLA2?(+/+) mice increased cardiac cPLA2 activity and urinary eicosanoid
excretion, decreased cardiac output, caused cardiovascular remodeling with
endothelial dysfunction, and increased vascular reactivity in cPLA2?(+/+) mice;
these changes were diminished in cPLA2?(-/-) mice. Angiotensin II also increased
cardiac infiltration of F4/80(+) macrophages and CD3(+) T lymphocytes,
cardiovascular oxidative stress, expression of endoplasmic reticulum stress
markers p58(IPK), and CHOP in cPLA2?(+/+) but not cPLA2?(-/-) mice. Angiotensin
II increased cardiac activity of ERK1/2 and cSrc in cPLA2?(+/+) but not
cPLA2?(-/-) mice. These data suggest that angiotensin II-induced hypertension and
associated cardiovascular pathophysiological changes are mediated by cPLA2?
activation, most likely through the release of arachidonic acid and generation of
eicosanoids with predominant prohypertensive effects and activation of ?1
signaling molecules, including ERK1/2 and cSrc.
|*Gene Expression Regulation
[MESH]
|*Oxidative Stress
[MESH]
|Angiotensin II/toxicity
[MESH]
|Animals
[MESH]
|Blood Pressure/*physiology
[MESH]
|Cytosol/*enzymology
[MESH]
|Disease Models, Animal
[MESH]
|Group IV Phospholipases A2/biosynthesis/*genetics
[MESH]
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