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10.1161/HYPERTENSIONAHA.114.04803 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.114.04803 C4359078!4359078!25667212     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25667212&cmd=llinks): Failed to open stream: HTTP request failed! 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CYTOSOLIC PHOSPHOLIPASE A2? IS CRITICAL FOR ANGIOTENSIN II ? INDUCED HYPERTENSION AND ASSOCIATED CARDIOVASCULAR PATHOPHYSIOLOGY |pdf=|usr=}}{{25667212}} gab.com Text CYTOSOLIC PHOSPHOLIPASE A2 IS CRITICAL FOR ANGIOTENSIN II INDUCED HYPERTENSION AND ASSOCIATED CARDIOVASCULAR PATHOPHYSIOLOGY JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25667212 #FOAvip Angiotensin II activates cPLA2? and releases arachidonic acid from tissue phospholipids which mediate or modulate one or more cardiovascular effects of angiotensin II and has been implicated in hypertension. Since 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 p58IPK 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 pro-hypertensive effects and activation of one or more signaling molecules including ERK1/2 and cSrc. Twit Text FOAVip CYTOSOLIC PHOSPHOLIPASE A2 IS CRITICAL FOR ANGIOTENSIN II INDUCED HYPERTENSION AND ASSOCIATED CARDIOVASCULAR PATHOPHYSIOLOGY ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25667212 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25667212 #FOAvip English Wikipedia <ref>{{Cite pmid|25667212}}</ref> 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 PMID25667212show ga Angiotensin II activates cPLA2? and releases arachidonic acid from tissue phospholipids which mediate or modulate one or more cardiovascular effects of angiotensin II and has been implicated in hypertension. Since 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 p58IPK 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 pro-hypertensive effects and activation of one or more signaling molecules including ERK1/2 and cSrc. äCYTOSOLIC PHOSPHOLIPASE A2? IS CRITICAL FOR ANGIOTENSIN II ? INDUCED H(epmc).pdf DeepDyve Pubget Overpricing